117 results on '"Misrani A"'
Search Results
2. Vibration-reduced anxiety-like behavior relies on ameliorating abnormalities of the somatosensory cortex and medial prefrontal cortex
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Afzal Misrani, Sidra Tabassum, Tintin Wang, Huixian Huang, Jinxiang Jiang, Hongjun Diao, Yanping Zhao, Zhen Huang, Shaohua Tan, Cheng Long, and Li Yang
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anxiety ,medial prefrontal cortex ,parvalbumin interneuron ,pressure ,somatosensory cortex ,tibetan singing bowl ,vibration ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
[INLINE:1] Tibetan singing bowls emit low-frequency sounds and produce perceptible harmonic tones and vibrations through manual tapping. The sounds the singing bowls produce have been shown to enhance relaxation and reduce anxiety. However, the underlying mechanism remains unclear. In this study, we used chronic restraint stress or sleep deprivation to establish mouse models of anxiety that exhibit anxiety-like behaviors. We then supplied treatment with singing bowls in a bottomless cage placed on the top of a cushion. We found that unlike in humans, the combination of harmonic tones and vibrations did not improve anxiety-like behaviors in mice, while individual vibration components did. Additionally, the vibration of singing bowls increased the level of N-methyl-D-aspartate receptor 1 in the somatosensory cortex and prefrontal cortex of the mice, decreased the level of γ-aminobutyric acid A (GABA) receptor α 1 subtype, reduced the level of CaMKII in the prefrontal cortex, and increased the number of GABAergic interneurons. At the same time, electrophysiological tests showed that the vibration of singing bowls significantly reduced the abnormal low-frequency gamma oscillation peak frequency in the medial prefrontal cortex caused by stress restraint pressure and sleep deprivation. Results from this study indicate that the vibration of singing bowls can alleviate anxiety-like behaviors by reducing abnormal molecular and electrophysiological events in somatosensory and medial prefrontal cortex.
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- 2024
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3. Resveratrol Attenuates Chronic Unpredictable Mild Stress-Induced Alterations in the SIRT1/PGC1α/SIRT3 Pathway and Associated Mitochondrial Dysfunction in Mice
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Tabassum, Sidra, Misrani, Afzal, Huang, Hui-xian, Zhang, Zai-yong, Li, Qiao-wei, and Long, Cheng
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- 2023
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4. Brain endothelial CD200 signaling protects brain against ischemic damage
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Afzal Misrani, Conelius Ngwa, Abdullah Al Mamun, Romana Sharmeen, Kanaka Valli Manyam, Rodney M. Ritzel, Louise McCullough, and Fudong Liu
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Endothelial CD200 ,Stroke ,BBB ,Neurological function ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Ischemic stroke induced inflammatory responses contribute significantly to neuronal damage and stroke outcomes. CD200 ligand and its receptor, CD200R, constitute an endogenous inhibitory signaling that is being increasingly recognized in studies of neuroinflammation in various central nervous system disorders. CD200 is a type 1 membrane glycoprotein that is broadly expressed by endothelia and neurons in the brain. In the present study, we have examined the role of endothelial CD200 signaling in acute ischemic stroke. Endothelial CD200 conditional knock out (CKO) mice were generated by breeding CD200 gene floxed mice with Cdh5Cre mice. The mice were subjected to a 60-min transient middle cerebral artery occlusion (MCAO). Flow cytometry, Immunohistochemical staining, and Western blotting were performed to assess the post-stroke inflammation; stroke outcomes (infarct volume and neurobehavioral deficits) were evaluated at 72 h after MCAO. We found CD200R was near-null expressed on microglia at 24 h after stoke. Endothelial CKO of CD200 had no impact on peripheral immune cell development. Immunohistochemical staining confirmed CD200 was expressed on CD200 floxed but not on CD200 CKO endothelia. CD200 CKO mice exhibited larger infarct size, worse neurological deficit scores (NDS), and more deficits in the adhesive removal when compared with control mice, 72 h after MCAO. Western blot results showed that endothelial CKO of CD200 did not change BBB protein expression. Together it suggests that endothelial CD200 signaling protects brains against ischemic injury through a mechanism not directly related to microglial activation.
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- 2024
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5. Brain endothelial CD200 signaling protects brain against ischemic damage
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Misrani, Afzal, Ngwa, Conelius, Mamun, Abdullah Al, Sharmeen, Romana, Manyam, Kanaka Valli, Ritzel, Rodney M., McCullough, Louise, and Liu, Fudong
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- 2024
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6. Minocycline Ameliorates Chronic Unpredictable Mild Stress-Induced Neuroinflammation and Abnormal mPFC-HIPP Oscillations in Mice
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Tabassum, Sidra, Misrani, Afzal, Huo, Qingwei, Ahmed, Adeel, Long, Cheng, and Yang, Li
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- 2022
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7. Systemic LPS-induced microglial activation results in increased GABAergic tone: A mechanism of protection against neuroinflammation in the medial prefrontal cortex in mice
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Jiang, Jinxiang, Tang, Binliang, Wang, Lei, Huo, Qingwei, Tan, Shuyi, Misrani, Afzal, Han, Yuanyuan, Li, Huidong, Hu, Haidong, Wang, Jichen, Cheng, Tinghui, Tabassum, Sidra, Chen, Ming, Xie, Wenyuan, Long, Cheng, and Yang, Li
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- 2022
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8. Abstract WP306: Endothelial CD200 Signaling Protects Brain Against Ischemic Damage
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Misrani, Afzal, primary, Ngwa, Conelius, additional, Mamun, Abdullah, additional, Ritzel, Rodney, additional, McCullough, Louise, additional, and Liu, Fudong, additional
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- 2024
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9. Enhancing GABAergic signaling ameliorates aberrant gamma oscillations of olfactory bulb in AD mouse models
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Ming Chen, Yunan Chen, Qingwei Huo, Lei Wang, Shuyi Tan, Afzal Misrani, Jinxiang Jiang, Jian Chen, Shiyuan Chen, Jiawei Zhang, Sidra Tabassum, Jichen Wang, Xi Chen, Cheng Long, and Li Yang
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Alzheimer’s disease ,APP/PS1 ,3xTg ,Olfactory bulb ,Gamma oscillations ,GABAAR ,Neurology. Diseases of the nervous system ,RC346-429 ,Geriatrics ,RC952-954.6 - Abstract
Abstract Background Before the deposition of amyloid-beta plaques and the onset of learning memory deficits, patients with Alzheimer’s disease (AD) experience olfactory dysfunction, typified by a reduced ability to detect, discriminate, and identify odors. Rodent models of AD, such as the Tg2576 and APP/PS1 mice, also display impaired olfaction, accompanied by aberrant in vivo or in vitro gamma rhythms in the olfactory pathway. However, the mechanistic relationships between the electrophysiological, biochemical and behavioral phenomena remain unclear. Methods To address the above issues in AD models, we conducted in vivo measurement of local field potential (LFP) with a combination of in vitro electro-olfactogram (EOG), whole-cell patch and field recordings to evaluate oscillatory and synaptic function and pharmacological regulation in the olfactory pathway, particularly in the olfactory bulb (OB). Levels of protein involved in excitation and inhibition of the OB were investigated by western blotting and fluorescence staining, while behavioral studies assessed olfaction and memory function. Results LFP measurements demonstrated an increase in gamma oscillations in the OB accompanied by altered olfactory behavior in both APP/PS1 and 3xTg mice at 3–5 months old, i.e. an age before the onset of plaque formation. Fewer olfactory sensory neurons (OSNs) and a reduced EOG contributed to a decrease in the excitatory responses of M/T cells, suggesting a decreased ability of M/T cells to trigger interneuron GABA release indicated by altered paired-pulse ratio (PPR), a presynaptic parameter. Postsynaptically, there was a compensatory increase in levels of GABAAR α1 and β3 subunits and subsequent higher amplitude of inhibitory responses. Strikingly, the GABA uptake inhibitor tiagabine (TGB) ameliorated abnormal gamma oscillations and levels of GABAAR subunits, suggesting a potential therapeutic strategy for early AD symptoms. These findings reveal increased gamma oscillations in the OB as a core indicator prior to onset of AD and uncover mechanisms underlying aberrant gamma activity in the OB. Conclusions This study suggests that the concomitant dysfunction of both olfactory behavior and gamma oscillations have important implications for early AD diagnosis: in particular, awareness of aberrant GABAergic signaling mechanisms might both aid diagnosis and suggest therapeutic strategies for olfactory damage in AD.
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- 2021
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10. Vibration-reduced anxiety-like behavior relies on ameliorating abnormalities of the somatosensory cortex and medial prefrontal cortex.
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Misrani, Afzal, Tabassum, Sidra, Tintin Wang, Huixian Huang, Jinxiang Jiang, Hongjun Diao, Yanping Zhao, Zhen Huang, Shaohua Tan, Cheng Long, and Li Yang
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- 2024
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11. Enhancing GABAergic signaling ameliorates aberrant gamma oscillations of olfactory bulb in AD mouse models
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Chen, Ming, Chen, Yunan, Huo, Qingwei, Wang, Lei, Tan, Shuyi, Misrani, Afzal, Jiang, Jinxiang, Chen, Jian, Chen, Shiyuan, Zhang, Jiawei, Tabassum, Sidra, Wang, Jichen, Chen, Xi, Long, Cheng, and Yang, Li
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- 2021
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12. Mitochondrial Deficits With Neural and Social Damage in Early-Stage Alzheimer’s Disease Model Mice
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Afzal Misrani, Sidra Tabassum, Qingwei Huo, Sumaiya Tabassum, Jinxiang Jiang, Adeel Ahmed, Xiangmao Chen, Jianwen Zhou, Jiajia Zhang, Sha Liu, Xiaoyi Feng, Cheng Long, and Li Yang
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Alzheimer’s disease ,hippocampus ,medial prefrontal cortex ,mitochondrial dynamics ,social interaction ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide. Mitochondrial dysfunction is thought to be an early event in the onset and progression of AD; however, the precise underlying mechanisms remain unclear. In this study, we investigated mitochondrial proteins involved in organelle dynamics, morphology and energy production in the medial prefrontal cortex (mPFC) and hippocampus (HIPP) of young (1∼2 months), adult (4∼5 months) and aged (9∼10, 12∼18 months) APP/PS1 mice. We observed increased levels of mitochondrial fission protein, Drp1, and decreased levels of ATP synthase subunit, ATP5A, leading to abnormal mitochondrial morphology, increased oxidative stress, glial activation, apoptosis, and altered neuronal morphology as early as 4∼5 months of age in APP/PS1 mice. Electrophysiological recordings revealed abnormal miniature excitatory postsynaptic current in the mPFC together with a minor connectivity change between the mPFC and HIPP, correlating with social deficits. These results suggest that abnormal mitochondrial dynamics, which worsen with disease progression, could be a biomarker of early-stage AD. Therapeutic interventions that improve mitochondrial function thus represent a promising approach for slowing the progression or delaying the onset of AD.
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- 2021
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13. Citalopram and its use in sleep-deprivation-induced depression
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Misrani, Afzal, primary and Long, Cheng, additional
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- 2021
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14. Contributors
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Abdollahi, Fatemeh, primary, Ahmed, Amani, additional, Alsaleh, Muaweah Ahmad, additional, Aydin, Efruz Pirdogan, additional, Barbosa-Méndez, Susana, additional, Batterham, Philip J., additional, Bayani Ershadi, Amir Sasan, additional, Becerril-Villanueva, Luis Enrique, additional, Bogucki, Olivia E., additional, Bris, Álvaro G., additional, Calear, Alison L., additional, Cardenas, Andres, additional, Carroll, Allison J., additional, Caso, Javier R., additional, Chaki, Shigeyuki, additional, Chan, Sally Wai-Chi, additional, Chattopadhyay, Ankita, additional, Dadfar, Mahboubeh, additional, Deriha, Kenta, additional, Diez-Quevedo, Crisanto, additional, dos Santos, Daniel Teixeira, additional, dos Santos Carvalho, Marco Aurélio, additional, Dozois, David J.A., additional, Ebrahimi-Ghiri, Mohaddeseh, additional, Ewais, Tatjana, additional, Faleschini, Sabrina, additional, Fekete, Andrea, additional, Fraguas, Renerio, additional, García Bueno, B., additional, García-Portilla, María Paz, additional, Gillies, Jennifer C.P., additional, Goes, Fernando S., additional, Gollan, Jacqueline K., additional, Gorenstein, Clarice, additional, Gortner, Isabel A., additional, Guimarães, Francisco, additional, Gupta, Girdhari Lal, additional, Hashimoto, Eri, additional, Hashimoto, Kenji, additional, Hatzigeorgiadis, Antonis, additional, Henna, Elaine, additional, Henriques, Vinícius Medeiros, additional, Hinz, Lisa D., additional, Hmwe, Nant Thin Thin, additional, Hollins Martin, Caroline J., additional, Hosseini, Mir-Jamal, additional, Hu, Bing, additional, Ibrahim, Normala, additional, Iglesias-González, Maria, additional, Joca, Samia, additional, Kawanishi, Chiaki, additional, Khakpai, Fatemeh, additional, Khosravi, Ahmad, additional, Kong, Jian, additional, Kurz, Ella, additional, de la Fuente-Tomás, Lorena, additional, Lai, Chien-Han, additional, Lee, Moon-Soo, additional, Lenart, Lilla, additional, Lester, David, additional, Leza, J.C., additional, Lisowska, Katarzyna A., additional, Long, Cheng, additional, Lusebrink, Vija B., additional, Lye, Munn-Sann, additional, MacDowell, K., additional, Madrigal, J.L.M., additional, Martin, Colin R., additional, Martin, Donel, additional, Martín-Hernández, David, additional, Matsuoka, Yutaka J., additional, Mesches, Gabrielle A., additional, Mignogna, Kristin, additional, Misrani, Afzal, additional, Morres, Ioannis D., additional, Mousavi, Seyed Abbas, additional, Nan, Joshua K.M., additional, Nikolin, Stevan, additional, Norman, Trevor R., additional, Okubo, Ryo, additional, Patil, Nikita, additional, Pellegrino, C., additional, Peng, Man-Man, additional, Pereira, Marta P., additional, Pietruczuk, Krzysztof, additional, Pingale, Tanvi, additional, Ponce-Regalado, María Dolores, additional, Ramezani, Somayeh, additional, Ran, Mao-Sheng, additional, Renemane, Lubova, additional, Rezzag, A., additional, Rivera, C., additional, Rohanachandra, Yasodha Maheshi, additional, Rong, Peijing, additional, de Sá Junior, Antonio Reis, additional, Sajdel-Sulkowska, Elizabeth M., additional, Salazar-Juárez, Alberto, additional, Sales, Amanda, additional, Sartim, Ariandra, additional, Semkovska, Maria, additional, Silote, Gabriela P., additional, de Souza, Bruno Pinatti Ferreira, additional, de Souza Paulo Filho, Guilherme, additional, Szałach, Łukasz P., additional, Talarowska, Monika, additional, Tessier, M., additional, Tey, Yin-Yee, additional, Theodorakis, Yannis, additional, Ukai, Wataru, additional, Ulecia-Morón, Cristina, additional, Uyar, Ece Turkyilmaz, additional, Vrublevska, Jelena, additional, Wang, Yuan-Pang, additional, Wegener, Gregers, additional, Weinstock, Marta, additional, Wilson, Georgia, additional, Xiao, Jinzhong, additional, Yamaguchi, Jun-ichi, additional, and Zhang, Kai, additional
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- 2021
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15. Differential effects of citalopram on sleep-deprivation-induced depressive-like behavior and memory impairments in mice
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Misrani, Afzal, Tabassum, Sidra, Chen, Xi, Tan, Shu-yi, Wang, Ji-chen, Yang, Li, and Long, Cheng
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- 2019
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16. Pelvic Pain Alters Functional Connectivity Between Anterior Cingulate Cortex and Hippocampus in Both Humans and a Rat Model
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Wenjun Yu, Xiaoyan Wu, Yunan Chen, Zhiying Liang, Jinxiang Jiang, Afzal Misrani, Yun Su, Yigang Peng, Jian Chen, Binliang Tang, Mengyao Sun, Cheng Long, Jun Shen, and Li Yang
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pelvic pain ,anterior cingulate cortex ,hippocampus ,neural circuits ,functional magnetic resonance imaging ,electrophysiology ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
The anterior cingulate cortex (ACC) and hippocampus (HIPP) are two key brain regions associated with pain and pain-related affective processing. However, whether and how pelvic pain alters the neural activity and connectivity of the ACC and HIPP under baseline and during social pain, and the underlying cellular and molecular mechanisms, remain unclear. Using functional magnetic resonance imaging (fMRI) combined with electrophysiology and biochemistry, we show that pelvic pain, particularly, primary dysmenorrhea (PDM), causes an increase in the functional connectivity between ACC and HIPP in resting-state fMRI, and a smaller reduction in connectivity during social exclusion in PDM females with periovulatory phase. Similarly, model rats demonstrate significantly increased ACC-HIPP synchronization in the gamma band, associating with reduced modulation by ACC-theta on HIPP-gamma and increased levels of receptor proteins and excitation. This study brings together human fMRI and animal research and enables improved therapeutic strategies for ameliorating pain and pain-related affective processing.
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- 2021
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17. Pigment of Ceiba speciosa (A. St.-Hil.) Flowers: Separation, Extraction, Purification and Antioxidant Activity
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Boyu Chen, Afzal Misrani, Cheng Long, Zhizhou He, Kun Chen, and Li Yang
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Ceiba speciosa ,pigment ,extraction ,purification ,lipopolysaccharide ,antioxidant ,Organic chemistry ,QD241-441 - Abstract
In this work, the extraction procedure of a natural pigment from the flower of Ceiba speciosa (A. St.-Hil.) was optimized by response surface methodology. It is the first time that the extraction of the flower pigment of C. speciosa (FPCS) has been reported, along with an evaluation of its stability and biological activity under various conditions, and an exploration of its potential use as a food additive and in medicine. Specifically, the effects of ethanol concentration, solid–liquid ratio, temperature and time on the extraction rate of FPCS were determined using a Box–Behnken design. The optimum extraction conditions for FPCS were 75% ethanol with a solid–liquid ratio of 1:75 mg/mL) at 66 °C for 39 min. The purification of FPCS using different macroporous resins showed that D101 performed best when the initial mass concentration of the injection solution was 1.50 mg/mL, resulting in a three-fold increase in color value. The yield of dry flowers was 9.75% of fresh petals and the FPCS extraction efficiency was 43.2%. The effects of light, solubility, pH, temperature, sweeteners, edible acids, redox agents, preservatives and metal ions on FPCS were also investigated. Furthermore, the characteristics of FPCS were determined by spectrophotometry at a specific wavelength using the Lambert–Beer law to correlate the mass of FPCS with its absorbance value. An acute toxicological test performed according to Horne’s method showed that FPCS is a non-toxic extract and thus may be used as a food additive or in other ingestible forms. Finally, western blotting showed that FPCS prevents lipopolysaccharide-induced hippocampal oxidative stress in mice. The study suggests that FPCS may function as an antioxidant with applications in the food, cosmetics and polymer industries.
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- 2022
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18. Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease
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Afzal Misrani, Sidra Tabassum, and Li Yang
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mitochondria ,oxidative stress ,fission ,fusion ,mitophagy ,Alzheimer’s disease ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Mitochondria play a pivotal role in bioenergetics and respiratory functions, which are essential for the numerous biochemical processes underpinning cell viability. Mitochondrial morphology changes rapidly in response to external insults and changes in metabolic status via fission and fusion processes (so-called mitochondrial dynamics) that maintain mitochondrial quality and homeostasis. Damaged mitochondria are removed by a process known as mitophagy, which involves their degradation by a specific autophagosomal pathway. Over the last few years, remarkable efforts have been made to investigate the impact on the pathogenesis of Alzheimer’s disease (AD) of various forms of mitochondrial dysfunction, such as excessive reactive oxygen species (ROS) production, mitochondrial Ca2+ dyshomeostasis, loss of ATP, and defects in mitochondrial dynamics and transport, and mitophagy. Recent research suggests that restoration of mitochondrial function by physical exercise, an antioxidant diet, or therapeutic approaches can delay the onset and slow the progression of AD. In this review, we focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of AD, emphasizing a framework of existing and potential therapeutic approaches.
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- 2021
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19. Exploiting Common Aspects of Obesity and Alzheimer’s Disease
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Sidra Tabassum, Afzal Misrani, and Li Yang
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obesity ,insulin resistance ,neuroinflammation ,Alzheimer’s disease ,mitochondrial dysfunction ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Alzheimer’s disease (AD) is an example of age-related dementia, and there are still no known preventive or curative measures for this disease. Obesity and associated metabolic changes are widely accepted as risk factors of age-related cognitive decline. Insulin is the prime mediator of metabolic homeostasis, which is impaired in obesity, and this impairment potentiates amyloid-β (Aβ) accumulation and the formation of neurofibrillary tangles (NFTs). Obesity is also linked with functional and morphological alterations in brain mitochondria leading to brain insulin resistance (IR) and memory deficits associated with AD. Also, increased peripheral inflammation and oxidative stress due to obesity are the main drivers that increase an individual’s susceptibility to cognitive deficits, thus doubling the risk of AD. This enhanced risk of AD is alarming in the context of a rapidly increasing global incidence of obesity and overweight in the general population. In this review, we summarize the risk factors that link obesity with AD and emphasize the point that the treatment and management of obesity may also provide a way to prevent AD.
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- 2020
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20. Resveratrol Attenuates Chronic Unpredictable Mild Stress-Induced Alterations in the SIRT1/PGC1α/SIRT3 Pathway and Associated Mitochondrial Dysfunction in Mice
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Sidra Tabassum, Afzal Misrani, Hui-xian Huang, Zai-yong Zhang, Qiao-wei Li, and Cheng Long
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Cellular and Molecular Neuroscience ,Neurology ,Neuroscience (miscellaneous) - Abstract
Environmental challenges, specifically chronic stress, have long been associated with neuropsychiatric disorders, including anxiety and depression. Sirtuin-1 (SIRT1) is a NAD+-dependent deacetylase that is widely distributed in the cortex and is involved in stress responses and neuropsychiatric disorders. Nevertheless, how chronic stress modulates the SIRT1 pathway and associated signaling remains unclear. In this study, we first explored the impact of chronic unpredictable mild stress (CUMS) on the SIRT1/PGC1α/SIRT3 pathway, on GABAergic mechanisms, and on mitophagy, autophagy and apoptosis in mice. We also asked whether activation of SIRT1 by resveratrol (RSV) can attenuate CUMS-induced molecular and behavioral alterations. Two-month-old C57/BL6J mice were subjected to three weeks of CUMS and one week of RSV treatment (30 mg/kg; i.p.) during the third week of CUMS. CUMS caused downregulation of the SIRT1/PGC1α/SIRT3 pathway leading to impaired mitochondrial morphology and function. CUMS also resulted in a reduction in numbers of parvalbumin-positive interneurons and increased oxidative stress leading to reduced expression of autophagy- and mitophagy-related proteins. Strikingly, activation of SIRT1 by RSV ameliorated expression of SIRT1/PGC1α/SIRT3, and also improved mitochondrial function, GABAergic mechanisms, mitophagy, autophagy and apoptosis. RSV also rescued CUMS-induced anxiety-like and depressive-like behavior in mice. Our results raise the compelling possibility that RSV treatment might be a viable therapeutic method of blocking stress-induced behavioral alterations.
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- 2023
21. Systemic LPS-induced microglial activation results in increased GABAergic tone: A mechanism of protection against neuroinflammation in the medial prefrontal cortex in mice
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Hui-dong Li, Afzal Misrani, Sidra Tabassum, Jinxiang Jiang, Shuyi Tan, Tinghui Cheng, Cheng Long, Yuanyuan Han, Wenyuan Xie, Li Yang, Jichen Wang, Qingwei Huo, Ming Chen, Binliang Tang, Hai-Dong Hu, and Lei Wang
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Lipopolysaccharides ,Endocrine and Autonomic Systems ,Chemistry ,Immunology ,Prefrontal Cortex ,Inhibitory postsynaptic potential ,Tail suspension test ,Mice, Inbred C57BL ,Mice ,Behavioral Neuroscience ,Glutamatergic ,Inhibitory Postsynaptic Potentials ,Downregulation and upregulation ,Neurotrophic factors ,Neuroinflammatory Diseases ,Animals ,GABAergic ,Microglia ,Prefrontal cortex ,Neuroscience ,Neuroinflammation - Abstract
Neuroinflammation with excess microglial activation and synaptic dysfunction are early symptoms of most neurological diseases. However, how microglia-associated neuroinflammation regulates synaptic activity remains obscure. We report here that acute neuroinflammation induced by intraperitoneal injection of lipopolysaccharide (LPS) results in cell-type-specific increases in inhibitory postsynaptic currents in the glutamatergic, but not the GABAergic, neurons of medial prefrontal cortex (mPFC), coinciding with excessive microglial activation. LPS causes upregulation in levels of GABAAR subunits, glutamine synthetase and vesicular GABA transporter, and downregulation in brain-derived neurotrophic factor (BDNF) and its receptor, pTrkB. Blockage of microglial activation by minocycline ameliorates LPS-induced abnormal expression of GABA signaling-related proteins and activity of synaptic and network. Moreover, minocycline prevents the mice from LPS-induced aberrant behavior, such as a reduction in total distance and time spent in the centre in the open field test; decreases in entries into the open arm of elevated-plus maze and in consumption of sucrose; increased immobility in the tail suspension test. Furthermore, upregulation of GABA signaling by tiagabine also prevents LPS-induced microglial activation and aberrant behavior. This study illustrates a mode of bidirectional constitutive signaling between the neural and immune compartments of the brain, and suggests that the mPFC is an important area for brain-immune system communication. Moreover, the present study highlights GABAergic signaling as a key therapeutic target for mitigating neuroinflammation-induced abnormal synaptic activity in the mPFC, together with the associated behavioral abnormalities.
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- 2022
22. Jujuboside A prevents sleep loss-induced disturbance of hippocampal neuronal excitability and memory impairment in young APP/PS1 mice
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Tabassum, Sidra, Misrani, Afzal, Tang, Bin-liang, Chen, Jian, Yang, Li, and Long, Cheng
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- 2019
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23. Resveratrol attenuates chronic unpredictable mild stress-induced alterations in the SIRT1/PGC1α/SIRT3 pathway and associated mitochondrial dysfunction in mice
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Tabassum, Sidra, primary, Misrani, Afzal, additional, Huang, Hui-xian, additional, Zhang, Zai-yong, additional, Li, Qiao-wei, additional, and Long, Cheng, additional
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- 2022
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24. Minocycline Ameliorates Chronic Unpredictable Mild Stress-Induced Neuroinflammation and Abnormal mPFC-HIPP Oscillations in Mice
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Sidra Tabassum, Afzal Misrani, Qingwei Huo, Adeel Ahmed, Cheng Long, and Li Yang
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Depression ,Neuroscience (miscellaneous) ,Prefrontal Cortex ,Minocycline ,Hippocampus ,Mitochondrial Proteins ,Cellular and Molecular Neuroscience ,Disease Models, Animal ,Mice ,Adenosine Triphosphate ,Neurology ,Glutamate-Ammonia Ligase ,Neuroinflammatory Diseases ,Animals ,Stress, Psychological ,gamma-Aminobutyric Acid - Abstract
Stress-induced neuroinflammation is a hallmark of modern society and has been linked to various emotional disorders, including anxiety. However, how microglia-associated neuroinflammation under chronic unpredictable mild stress (CUMS) alters mitochondrial function and subsequent medial prefrontal cortex-hippocampus (mPFC-HIPP) connectivity remains obscure. We speculated that CUMS might induce neuroinflammation, which involves altered mitochondrial protein levels, blockade of neuroinflammation by a microglial modulator, minocycline, protects against CUMS-induced alterations. Mice were exposed to CUMS for 3 weeks and received minocycline (50 mg/kg) intraperitoneally for 7 consecutive days during the 3
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- 2022
25. Pigment of
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Boyu, Chen, Afzal, Misrani, Cheng, Long, Zhizhou, He, Kun, Chen, and Li, Yang
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Ceiba ,Mice ,Ethanol ,Plant Extracts ,Animals ,Food Additives ,Flowers ,Antioxidants - Abstract
In this work, the extraction procedure of a natural pigment from the flower of
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- 2022
26. Pigment of Ceiba speciosa (A. St.-Hil.) Flowers: Separation, Extraction, Purification and Antioxidant Activity
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Chen, Boyu, primary, Misrani, Afzal, additional, Long, Cheng, additional, He, Zhizhou, additional, Chen, Kun, additional, and Yang, Li, additional
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- 2022
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27. Effect of microRNA-455-5p (miR-455-5p) on the Expression of the Cytokine Signaling-3 (SOCS3) Gene During Myocardial Infarction
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Zaiyong Zhang, Wenzhi Luo, Yuanyuan Han, Afzal Misrani, Hanwei Chen, and Cheng Long
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digestive, oral, and skin physiology ,Biomedical Engineering ,Myocardial Infarction ,Pharmaceutical Science ,Medicine (miscellaneous) ,Bioengineering ,Apoptosis ,Hydrogen Peroxide ,MicroRNAs ,Suppressor of Cytokine Signaling 3 Protein ,Cytokines ,Humans ,General Materials Science ,Myocytes, Cardiac - Abstract
To explore the effect of microRNA-455-5p (miR-455-5p) and Cytokine Signaling-3 (SOCS3) expression, a model of the cell damage induced during myocardial infarction was established using H2O2. The cell counting Kit-8 (CCK-8) and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) assays were used to detect the cell viability and the expression of miR-455-5p and SOCS3 in cells cultured with different concentrations of H2O2. After the selection of the optimum culture concentration, a dual-luciferase reporter gene assay was used to detect the binding between and miR-455-5p and its potential target SOCS3. SOCS3 siRNA was transfected into cardiomyocytes using chitosan nanoparticles as a gene carrier, which led to the knockdown of SOCS3 expression, and the cells were transfected with miR-455-5p mimics and inhibitors. The expression of cardiac protective proteins was detected by western blotting, cell viability was detected by CCK8, and cell apoptosis was detected by flow cytometry. The aim of this study was to investigate the effect of miR-455-5p and SOCS3 expression on the activity and apoptosis of damaged cardiomyocytes, and to identify any protective effect on cardiomyocytes. Finally, after the simultaneous overexpression of SOCS3 and miR-455-5p, and the expression of cardiac protective proteins, cell activity, and apoptosis rate were detected. The results showed that the expression of miR-455-5p decreased in a concentration-dependent manner and that the expression of SOCS3 increased in a concentration-dependent manner when the cells were cultured in different concentrations of H2O2. The knockdown of SOCS3 expression promoted an increase in cell activity, an increase in cardiac protective proteins, and a decrease in apoptosis. The upregulation of miR-455-5p significantly inhibited the expression of SOCS3, increased cell activity, inhibited apoptosis, and exerted protective effects in myocardial cells. The overexpression of SOCS3 reversed the inhibition of SOCS3 by miR-455-5p and reduced the protective effect of miR-455-5p on myocardial cells. Therefore, this study showed that the upregulation of miR-455-5p significantly inhibited the expression of SOCS3 and resulted in the increased protection of cells damaged by H2O2, which was used as a model of myocardial infarction. These results indicate the potential of miR-455-5p in myocardial protection, suggesting that miRNA may be a resource for myocardial therapy.
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- 2022
28. Regulatory Mechanism of circEIF4G2 Targeting miR-26a in Acute Myocardial Infarction
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Zaiyong Zhang, Jianhao Li, Cheng Long, Yuanyuan Han, Jun Fan, Afzal Misrani, and Xiangyu Ji
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Vascular Endothelial Growth Factor A ,MicroRNAs ,Article Subject ,Neovascularization, Pathologic ,Biomedical Engineering ,Human Umbilical Vein Endothelial Cells ,Myocardial Infarction ,Humans ,Health Informatics ,Surgery ,Biotechnology ,Cell Proliferation - Abstract
Background. Acute myocardial infarction (AMI) involves a series of complex cellular and molecular events, including circular RNAs (circRNAs), microRNAs (miRNAs) and other noncoding RNAs. Objective. In this study, the regulation mechanism of circEIF4G2 acting on miR-26a on HUVECs (Human Umbilical Vein Endothelial Cells) proliferation, cell cycle and angiogenesis ability was mainly explored in the vascular endothelial growth factor induced (VEGF-induced) angiogenesis model. Methods. VEGF induced HUVECs angiogenesis model was constructed, and the expression of circEIF4G2 and miR-26a in VEGF model was detected by qRT-PCR. When circEIF4G2 and miR-26a were knocked down or overexpressed in HUVECs, qRT-PCR was used to detect the expression of circEIF4G2 and miR-26a, CCK-8 was used to detect cell proliferation, flow cytometry was used to detect the cell cycle transition of HUVECs, and cell formation experiment was used to detect the ability of angiogenesis. MiRanda database and Targetscan predicted the binding site of circEIF4G2 and miR-26a, lucifase reporting assay and RNA pull down assay verified the interaction between circEIF4G2 and miR-26a. Results. After HUVECs were treated with VEGF, circEIF4G2 was significantly upregulated. After circEIF4G2 was knocked down, the proliferation and angiogenesis of HUVECs cells were decreased, and the process of cell cycle G0/G1 phase was blocked. The overexpression of miR-26a reduced the proliferation and angiogenesis of HUVECs cells and blocked the cell cycle progression of G0/G1 phase. Double lucifase reporter gene assay verified that circEIF4G2 could directly interact with miR-26a through the binding site, and RNA Pull down assay further verified the interaction between circEIF4G2 and miR-26a. When circEIF4G2 and miR-26a were knocked down simultaneously in HUVECs, it was found that knocking down miR-26a could reverse the inhibition of circEIF4G2 on cell proliferation, cycle and angiogenesis. Conclusion. In the VEGF model, circEIF4G2 was highly expressed and miR-26a was low expressed. MiR-26a regulates HUVECs proliferation, cycle and angiogenesis by targeting circEIF4G2.
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- 2022
29. Regulatory Mechanism of circEIF4G2 Targeting miR-26a in Acute Myocardial Infarction
- Author
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Zhang, Zaiyong, primary, Li, Jianhao, additional, Long, Cheng, additional, Han, Yuanyuan, additional, Fan, Jun, additional, Misrani, Afzal, additional, and Ji, Xiangyu, additional
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- 2022
- Full Text
- View/download PDF
30. Analisis Layanan Penerimaan Berkas Pencairan Santunan Kematian Di Kecamatan Kluet Timur
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Misrani, Misrani, primary, Fadhly, Zuhrizal, additional, and Anisullah, Anisullah, additional
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- 2022
- Full Text
- View/download PDF
31. Effect of microRNA-455-5p (miR-455-5p) on the Expression of the Cytokine Signaling-3 (SOCS3) Gene During Myocardial Infarction
- Author
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Zhang, Zaiyong, primary, Luo, Wenzhi, additional, Han, Yuanyuan, additional, Misrani, Afzal, additional, Chen, Hanwei, additional, and Long, Cheng, additional
- Published
- 2022
- Full Text
- View/download PDF
32. Citalopram prevents sleep-deprivation-induced reduction in CaMKII-CREB-BDNF signaling in mouse prefrontal cortex
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Sidra Tabassum, Meng Wang, Cheng Long, Li Yang, Afzal Misrani, and Jian Chen
- Subjects
Male ,0301 basic medicine ,medicine.medical_specialty ,Prefrontal Cortex ,Citalopram ,CREB ,Neuroprotection ,03 medical and health sciences ,0302 clinical medicine ,Postsynaptic potential ,Neurotrophic factors ,Ca2+/calmodulin-dependent protein kinase ,Internal medicine ,medicine ,Animals ,Patch clamp ,Cyclic AMP Response Element-Binding Protein ,Prefrontal cortex ,biology ,business.industry ,Brain-Derived Neurotrophic Factor ,Pyramidal Cells ,General Neuroscience ,Miniature Postsynaptic Potentials ,Mice, Inbred C57BL ,030104 developmental biology ,Endocrinology ,biology.protein ,Excitatory postsynaptic potential ,Antidepressive Agents, Second-Generation ,Sleep Deprivation ,Female ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,business ,030217 neurology & neurosurgery ,Signal Transduction - Abstract
Curtailment of sleep in modern society leads to a spectrum of neuropsychiatric disorders. However, the molecular mechanisms underlying the effects of sleep deprivation (SD) remain elusive and currently there is no effective therapy to alleviate these effects. Here, we aimed to examine SD-induced cellular and molecular alterations in mouse prefrontal cortex (PFC) and whether subchronic citalopram (CTM) treatment can negate these alterations. Three-month-old C57BL/6 J mice were divided into control (Ctrl), SD, CTM alone and CTM + SD groups. CTM and CTM + SD group mice were treated with CTM for five consecutive days at a dose of 10 mg/kg per day before the experimental procedure. SD and CTM + SD group mice were sleep-deprived for 24 h using an automated treadmill method. We found that 24 h SD causes a marked reduction in the levels of phosphorylated calcium/calmodulin kinase II (pCaMKII), phosphorylated cyclic AMP-responsive element binding protein (pCREB) and brain-derived neurotrophic factor (BDNF) in mouse PFC. Patch clamp recording of pyramidal neurons from acute PFC slices revealed that SD decreases the amplitude of miniature excitatory postsynaptic currents (mEPSCs), suggesting a SD-induced postsynaptic alteration. Interestingly, subchronic CTM treatment prevents such SD-induced reductions in pCaMKII, pCREB and BDNF levels, and in mEPSC amplitude. These data suggest that CTM offers neuroprotection against SD-induced molecular and electrophysiological alterations.
- Published
- 2020
33. Mitochondrial Deficits With Neural and Social Damage in Early-Stage Alzheimer’s Disease Model Mice
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Misrani, Afzal, primary, Tabassum, Sidra, additional, Huo, Qingwei, additional, Tabassum, Sumaiya, additional, Jiang, Jinxiang, additional, Ahmed, Adeel, additional, Chen, Xiangmao, additional, Zhou, Jianwen, additional, Zhang, Jiajia, additional, Liu, Sha, additional, Feng, Xiaoyi, additional, Long, Cheng, additional, and Yang, Li, additional
- Published
- 2021
- Full Text
- View/download PDF
34. Minocycline inhibits sleep deprivation-induced aberrant microglial activation and Keap1-Nrf2 expression in mouse hippocampus
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Ahmed, Adeel, primary, Misrani, Afzal, additional, Tabassum, Sidra, additional, Yang, Li, additional, and Long, Cheng, additional
- Published
- 2021
- Full Text
- View/download PDF
35. Mitophagy pathways and Alzheimer's disease: From pathogenesis to treatment
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Pan, Xian-Ji, primary, Misrani, Afzal, additional, Tabassum, Sidra, additional, and Yang, Li, additional
- Published
- 2021
- Full Text
- View/download PDF
36. Enhancing GABAergic signaling ameliorates aberrant gamma oscillations of olfactory bulb in AD mouse models
- Author
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Jia-wei Zhang, Shuyi Tan, Xi Chen, Jian Chen, Afzal Misrani, Shiyuan Chen, Qingwei Huo, Jinxiang Jiang, Ming Chen, Cheng Long, Li Yang, Jichen Wang, Yunan Chen, Sidra Tabassum, and Lei Wang
- Subjects
Male ,0301 basic medicine ,Olfactory system ,Interneuron ,Plaque, Amyloid ,Sensory system ,Olfaction ,lcsh:Geriatrics ,Biology ,Inhibitory postsynaptic potential ,lcsh:RC346-429 ,Mice ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,Olfactory bulb ,0302 clinical medicine ,Alzheimer Disease ,medicine ,Animals ,Gamma Rhythm ,Humans ,GABAergic Neurons ,Tiagabine ,Molecular Biology ,Gamma oscillations ,lcsh:Neurology. Diseases of the nervous system ,APP/PS1 ,GABAAR ,Amyloid beta-Peptides ,3xTg ,Smell ,Disease Models, Animal ,lcsh:RC952-954.6 ,030104 developmental biology ,medicine.anatomical_structure ,Excitatory postsynaptic potential ,GABAergic ,Female ,Neurology (clinical) ,Alzheimer’s disease ,Neuroscience ,030217 neurology & neurosurgery ,Research Article - Abstract
Background Before the deposition of amyloid-beta plaques and the onset of learning memory deficits, patients with Alzheimer’s disease (AD) experience olfactory dysfunction, typified by a reduced ability to detect, discriminate, and identify odors. Rodent models of AD, such as the Tg2576 and APP/PS1 mice, also display impaired olfaction, accompanied by aberrant in vivo or in vitro gamma rhythms in the olfactory pathway. However, the mechanistic relationships between the electrophysiological, biochemical and behavioral phenomena remain unclear. Methods To address the above issues in AD models, we conducted in vivo measurement of local field potential (LFP) with a combination of in vitro electro-olfactogram (EOG), whole-cell patch and field recordings to evaluate oscillatory and synaptic function and pharmacological regulation in the olfactory pathway, particularly in the olfactory bulb (OB). Levels of protein involved in excitation and inhibition of the OB were investigated by western blotting and fluorescence staining, while behavioral studies assessed olfaction and memory function. Results LFP measurements demonstrated an increase in gamma oscillations in the OB accompanied by altered olfactory behavior in both APP/PS1 and 3xTg mice at 3–5 months old, i.e. an age before the onset of plaque formation. Fewer olfactory sensory neurons (OSNs) and a reduced EOG contributed to a decrease in the excitatory responses of M/T cells, suggesting a decreased ability of M/T cells to trigger interneuron GABA release indicated by altered paired-pulse ratio (PPR), a presynaptic parameter. Postsynaptically, there was a compensatory increase in levels of GABAAR α1 and β3 subunits and subsequent higher amplitude of inhibitory responses. Strikingly, the GABA uptake inhibitor tiagabine (TGB) ameliorated abnormal gamma oscillations and levels of GABAAR subunits, suggesting a potential therapeutic strategy for early AD symptoms. These findings reveal increased gamma oscillations in the OB as a core indicator prior to onset of AD and uncover mechanisms underlying aberrant gamma activity in the OB. Conclusions This study suggests that the concomitant dysfunction of both olfactory behavior and gamma oscillations have important implications for early AD diagnosis: in particular, awareness of aberrant GABAergic signaling mechanisms might both aid diagnosis and suggest therapeutic strategies for olfactory damage in AD.
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- 2021
37. Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease
- Author
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Li Yang, Afzal Misrani, and Sidra Tabassum
- Subjects
0301 basic medicine ,Aging ,fusion ,Bioenergetics ,Cognitive Neuroscience ,Review ,Biology ,Mitochondrion ,medicine.disease_cause ,lcsh:RC321-571 ,Pathogenesis ,03 medical and health sciences ,0302 clinical medicine ,Mitophagy ,medicine ,oxidative stress ,fission ,Viability assay ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,chemistry.chemical_classification ,Reactive oxygen species ,Cell biology ,mitochondria ,030104 developmental biology ,mitophagy ,chemistry ,Alzheimer’s disease ,030217 neurology & neurosurgery ,Homeostasis ,Oxidative stress ,Neuroscience - Abstract
Mitochondria play a pivotal role in bioenergetics and respiratory functions, which are essential for the numerous biochemical processes underpinning cell viability. Mitochondrial morphology changes rapidly in response to external insults and changes in metabolic status via fission and fusion processes (so-called mitochondrial dynamics) that maintain mitochondrial quality and homeostasis. Damaged mitochondria are removed by a process known as mitophagy, which involves their degradation by a specific autophagosomal pathway. Over the last few years, remarkable efforts have been made to investigate the impact on the pathogenesis of Alzheimer’s disease (AD) of various forms of mitochondrial dysfunction, such as excessive reactive oxygen species (ROS) production, mitochondrial Ca2+ dyshomeostasis, loss of ATP, and defects in mitochondrial dynamics and transport, and mitophagy. Recent research suggests that restoration of mitochondrial function by physical exercise, an antioxidant diet, or therapeutic approaches can delay the onset and slow the progression of AD. In this review, we focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of AD, emphasizing a framework of existing and potential therapeutic approaches.
- Published
- 2021
38. Mitophagy pathways and Alzheimer's disease: From pathogenesis to treatment
- Author
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Li Yang, Xian-Ji Pan, Afzal Misrani, and Sidra Tabassum
- Subjects
0301 basic medicine ,Cell ,tau Proteins ,Disease ,Mitochondrion ,Pathogenesis ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Alzheimer Disease ,Lysosome ,Mitophagy ,medicine ,Animals ,Humans ,Disease process ,Phosphorylation ,Molecular Biology ,Amyloid beta-Peptides ,Cellular process ,business.industry ,Cell Biology ,Mitochondria ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Gene Expression Regulation ,Disease Progression ,Molecular Medicine ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Alzheimer's disease (AD) is an age-dependent, incurable mental illness that is associated with the accumulation of aggregates of amyloid-beta (Aβ) and hyperphosphorylated tau fragments (p-tau). Detailed studies on postmortem AD brains, cell lines, and mouse models of AD have shown that numerous cellular alterations, including mitochondrial deficits, synaptic disruption and glial/astrocytic activation, are involved in the disease process. Mitophagy is a cellular process by which damaged/weakened mitochondria are selectively eliminated from the cell. In AD, impairments in mitophagy trigger the gradual accumulation of defective mitochondria. This review will focus on the recent progress in understanding the molecular mechanisms and pathological role of mitophagy and its implications for AD pathogenesis. We will also discuss the novel concept of the regulation of mitophagy as a therapeutic avenue for the prevention and treatment of AD.
- Published
- 2021
39. Minocycline inhibits sleep deprivation-induced aberrant microglial activation and Keap1-Nrf2 expression in mouse hippocampus
- Author
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Sidra Tabassum, Cheng Long, Li Yang, Adeel Ahmed, and Afzal Misrani
- Subjects
0301 basic medicine ,Male ,Elevated plus maze ,medicine.medical_specialty ,NF-E2-Related Factor 2 ,Hippocampus ,Minocycline ,Anxiety ,Open field ,03 medical and health sciences ,Mice ,0302 clinical medicine ,In vivo ,Internal medicine ,medicine ,Animals ,Neuroinflammation ,Swimming ,Kelch-Like ECH-Associated Protein 1 ,Microglia ,Behavior, Animal ,business.industry ,Depression ,General Neuroscience ,Anti-Inflammatory Agents, Non-Steroidal ,Electroencephalography ,Macrophage Activation ,Mice, Inbred C57BL ,Sleep deprivation ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,Hindlimb Suspension ,Sleep Deprivation ,Female ,medicine.symptom ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Sleep deprivation (SD) is a hallmark of modern society and associated with many neuropsychiatric disorders, including depression and anxiety. However, the cellular and molecular mechanisms underlying SD-associated depression and anxiety remain elusive. Does the neuroinflammation play a role in mediating the effects of SD? In this study, we investigated SD-induced cellular and molecular alterations in the hippocampus and asked whether treatment with an anti-inflammatory drug, minocycline, could attenuate these alterations. We found that SD animals exhibit activated microglia and decreased levels of Keap1 and Nrf2 (antioxidant and anti-inflammatory factors) in the hippocampus. In vivo local field potential recordings show decreased theta and beta oscillations, but increased high gamma oscillations, as a result of SD. Behavioral analysis revealed increased immobility time in the forced swim and tail suspension tests, and decreased sucrose intake in SD mice, all indicative of depressive-like behavior. Moreover, open field test and elevated plus maze test results indicated that SD increases anxiety-like behavior. Interestingly, treatment with the microglial modulator minocycline prevented SD-induced microglial activation, restored Keap1 and Nrf2 levels, normalized neuronal oscillations, and alleviated depressive-like and anxiety-like behavior. The present study reveals that microglial activation and Keap1-Nrf2 signaling play a crucial role in SD-induced behavioral alteration, and that minocycline treatment has a protective effect on these alterations.
- Published
- 2021
40. Contributors
- Author
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Fatemeh Abdollahi, Amani Ahmed, Muaweah Ahmad Alsaleh, Efruz Pirdogan Aydin, Susana Barbosa-Méndez, Philip J. Batterham, Amir Sasan Bayani Ershadi, Luis Enrique Becerril-Villanueva, Olivia E. Bogucki, Álvaro G. Bris, Alison L. Calear, Andres Cardenas, Allison J. Carroll, Javier R. Caso, Shigeyuki Chaki, Sally Wai-Chi Chan, Ankita Chattopadhyay, Mahboubeh Dadfar, Kenta Deriha, Crisanto Diez-Quevedo, Daniel Teixeira dos Santos, Marco Aurélio dos Santos Carvalho, David J.A. Dozois, Mohaddeseh Ebrahimi-Ghiri, Tatjana Ewais, Sabrina Faleschini, Andrea Fekete, Renerio Fraguas, B. García Bueno, María Paz García-Portilla, Jennifer C.P. Gillies, Fernando S. Goes, Jacqueline K. Gollan, Clarice Gorenstein, Isabel A. Gortner, Francisco Guimarães, Girdhari Lal Gupta, Eri Hashimoto, Kenji Hashimoto, Antonis Hatzigeorgiadis, Elaine Henna, Vinícius Medeiros Henriques, Lisa D. Hinz, Nant Thin Thin Hmwe, Caroline J. Hollins Martin, Mir-Jamal Hosseini, Bing Hu, Normala Ibrahim, Maria Iglesias-González, Samia Joca, Chiaki Kawanishi, Fatemeh Khakpai, Ahmad Khosravi, Jian Kong, Ella Kurz, Lorena de la Fuente-Tomás, Chien-Han Lai, Moon-Soo Lee, Lilla Lenart, David Lester, J.C. Leza, Katarzyna A. Lisowska, Cheng Long, Vija B. Lusebrink, Munn-Sann Lye, K. MacDowell, J.L.M. Madrigal, Colin R. Martin, Donel Martin, David Martín-Hernández, Yutaka J. Matsuoka, Gabrielle A. Mesches, Kristin Mignogna, Afzal Misrani, Ioannis D. Morres, Seyed Abbas Mousavi, Joshua K.M. Nan, Stevan Nikolin, Trevor R. Norman, Ryo Okubo, Nikita Patil, C. Pellegrino, Man-Man Peng, Marta P. Pereira, Krzysztof Pietruczuk, Tanvi Pingale, María Dolores Ponce-Regalado, Somayeh Ramezani, Mao-Sheng Ran, Lubova Renemane, A. Rezzag, C. Rivera, Yasodha Maheshi Rohanachandra, Peijing Rong, Antonio Reis de Sá Junior, Elizabeth M. Sajdel-Sulkowska, Alberto Salazar-Juárez, Amanda Sales, Ariandra Sartim, Maria Semkovska, Gabriela P. Silote, Bruno Pinatti Ferreira de Souza, Guilherme de Souza Paulo Filho, Łukasz P. Szałach, Monika Talarowska, M. Tessier, Yin-Yee Tey, Yannis Theodorakis, Wataru Ukai, Cristina Ulecia-Morón, Ece Turkyilmaz Uyar, Jelena Vrublevska, Yuan-Pang Wang, Gregers Wegener, Marta Weinstock, Georgia Wilson, Jinzhong Xiao, Jun-ichi Yamaguchi, and Kai Zhang
- Published
- 2021
41. Citalopram and its use in sleep-deprivation-induced depression
- Author
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Cheng Long and Afzal Misrani
- Subjects
business.industry ,Serotonin reuptake inhibitor ,Citalopram ,Sleep in non-human animals ,Sleep deprivation ,Mood ,Neuroplasticity ,Synaptic plasticity ,medicine ,Antidepressant ,medicine.symptom ,business ,Neuroscience ,medicine.drug - Abstract
Curtailment of sleep in modern society leads to a spectrum of neuropsychiatric disorders. Mounting evidence suggests that sleep deprivation (SD) is a risk factor for depression. Most recently, various reports have revealed the role of sleep in neuronal plasticity, learning and memory, and mood. SD studies provide insights into the cellular and molecular processes that are sensitive to sleep loss and have shown that SD negatively affects various brain regions. Citalopram (CTM), a selective serotonin reuptake inhibitor (SSRI), is the most-frequently used antidepressant in clinical practice. The identification of an SD-induced impairment in the CaMKII-CREB-BDNF signaling pathway, which is implicated in synaptic plasticity and the beneficial effects of CTM on this pathway represent a novel treatment target for neuropsychiatric disorders associated with sleep loss. In this chapter, we provide an overview of CTM use in SD-induced depression.
- Published
- 2021
42. Additional file 1 of Enhancing GABAergic signaling ameliorates aberrant gamma oscillations of olfactory bulb in AD mouse models
- Author
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Chen, Ming, Yunan Chen, Qingwei Huo, Wang, Lei, Shuyi Tan, Misrani, Afzal, Jinxiang Jiang, Chen, Jian, Shiyuan Chen, Jiawei Zhang, Sidra Tabassum, Jichen Wang, Chen, Xi, Long, Cheng, and Yang, Li
- Abstract
Additional file 1: Original Western blotting results.
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- 2021
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43. Pelvic Pain Alters Functional Connectivity Between Anterior Cingulate Cortex and Hippocampus in Both Humans and a Rat Model
- Author
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Yu, Wenjun, primary, Wu, Xiaoyan, additional, Chen, Yunan, additional, Liang, Zhiying, additional, Jiang, Jinxiang, additional, Misrani, Afzal, additional, Su, Yun, additional, Peng, Yigang, additional, Chen, Jian, additional, Tang, Binliang, additional, Sun, Mengyao, additional, Long, Cheng, additional, Shen, Jun, additional, and Yang, Li, additional
- Published
- 2021
- Full Text
- View/download PDF
44. Exploiting Common Aspects of Obesity and Alzheimer’s Disease
- Author
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Afzal Misrani, Sidra Tabassum, and Li Yang
- Subjects
obesity ,Population ,Context (language use) ,Review ,Disease ,Overweight ,Bioinformatics ,Management of obesity ,lcsh:RC321-571 ,neuroinflammation ,03 medical and health sciences ,Behavioral Neuroscience ,0302 clinical medicine ,Insulin resistance ,insulin resistance ,mitochondrial dysfunction ,medicine ,Dementia ,Cognitive decline ,education ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Biological Psychiatry ,030304 developmental biology ,0303 health sciences ,education.field_of_study ,business.industry ,Human Neuroscience ,medicine.disease ,Psychiatry and Mental health ,Neuropsychology and Physiological Psychology ,Neurology ,medicine.symptom ,business ,Alzheimer’s disease ,030217 neurology & neurosurgery - Abstract
Alzheimer’s disease (AD) is an example of age-related dementia, and there are still no known preventive or curative measures for this disease. Obesity and associated metabolic changes are widely accepted as risk factors of age-related cognitive decline. Insulin is the prime mediator of metabolic homeostasis, which is impaired in obesity, and this impairment potentiates amyloid-β (Aβ) accumulation and the formation of neurofibrillary tangles (NFTs). Obesity is also linked with functional and morphological alterations in brain mitochondria leading to brain insulin resistance (IR) and memory deficits associated with AD. Also, increased peripheral inflammation and oxidative stress due to obesity are the main drivers that increase an individual’s susceptibility to cognitive deficits, thus doubling the risk of AD. This enhanced risk of AD is alarming in the context of a rapidly increasing global incidence of obesity and overweight in the general population. In this review, we summarize the risk factors that link obesity with AD and emphasize the point that the treatment and management of obesity may also provide a way to prevent AD.
- Published
- 2020
45. Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease
- Author
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Misrani, Afzal, primary, Tabassum, Sidra, additional, and Yang, Li, additional
- Published
- 2021
- Full Text
- View/download PDF
46. Disrupted prefrontal neuronal oscillations and morphology induced by sleep deprivation in young APP/PS1 transgenic AD mice
- Author
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Tabassum, Sidra, primary, Misrani, Afzal, additional, Tabassum, Sumaiya, additional, Ahmed, Adeel, additional, Yang, Li, additional, and Long, Cheng, additional
- Published
- 2021
- Full Text
- View/download PDF
47. Microglial activation results in neuron-type-specific increase in mPFC GABAergic transmission and abnormal behavior in mice
- Author
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Afzal Misrani, Qingwei Huo, Binliang Tang, Jinxiang Jiang, Cheng Long, Li Yang, Lei Wang, and Yuanyuan Han
- Subjects
Glutamatergic ,medicine.anatomical_structure ,Microglia ,Chemistry ,medicine ,GABAergic ,Signal transduction ,Prefrontal cortex ,Inhibitory postsynaptic potential ,Neuroscience ,Neuroinflammation ,Proinflammatory cytokine - Abstract
Neuroinflammation and synaptic dysfunction are two early symptoms of most neurological diseases. However, the mechanisms underlying microglia-associated neuroinflammation in the regulation of synaptic activity remain obscure. We report here that acute neuroinflammation induced by a single-dose proinflammatory cytokine inducer, lipopolysaccharide (LPS), results in enhanced inhibitory postsynaptic currents (IPSCs) of glutamatergic neurons, upregulated levels of GABAAR subunits, glutamine synthetase (GS) and vGAT, and downregulated BDNF and pTrkB levels, due to enhanced activation of microglia in the medial prefrontal cortex (mPFC). Blockage of microglial activation by minocycline ameliorated LPS-induced aberrant mIPSCs and associated aberrant protein expression and behavior. Exogenous application of BDNF prior to LPS challenge also ameliorated LPS-induced abnormal mIPSCs. Thus, this study elucidates a critical role for microglia in the neurobiology of GABAergic synaptic dysfunction induced by neuroinflammation, revealing a novel GABAergic signaling pathway that might be targeted therapeutically to treat neuroinflammation-induced abnormal synaptic activity and associated aberrant behavior.
- Published
- 2020
48. Disrupted prefrontal neuronal oscillations and morphology induced by sleep deprivation in young APP/PS1 transgenic AD mice
- Author
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Afzal Misrani, Cheng Long, Sumaiya Tabassum, Li Yang, Sidra Tabassum, and Adeel Ahmed
- Subjects
0301 basic medicine ,Prefrontal Cortex ,Mice, Transgenic ,CREB ,Neuroprotection ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Postsynaptic potential ,Alzheimer Disease ,Ca2+/calmodulin-dependent protein kinase ,Medicine ,Animals ,Prefrontal cortex ,biology ,business.industry ,General Neuroscience ,Excitatory Postsynaptic Potentials ,Brain Waves ,Sleep deprivation ,030104 developmental biology ,nervous system ,Excitatory postsynaptic potential ,biology.protein ,NMDA receptor ,Sleep Deprivation ,medicine.symptom ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Emerging evidence suggests that sleep deprivation (SD) is a public health epidemic and increase the risk of Alzheimer's disease (AD) progression. However, the underlying mechanisms remain to be fully investigated. In this study, we investigate the impact of 72 h SD on the prefrontal cortex (PFC) of 3∼4-months-old APP/PS1 transgenic AD mice - at an age before the onset of plaque formation and memory decline. Our results reveal that SD alters delta, theta and high-gamma oscillations in the PFC, accompanied by increased levels of excitatory postsynaptic signaling (NMDAR, GluR1, and CaMKII) in AD mice. SD also caused alteration in the dendritic length and dendritic branches of PFC pyramidal neurons, accompanied by a reduction in neuroprotective agent CREB. This study suggests that failure to acquire adequate sleep could trigger an early electrophysiological, molecular, and morphological alteration in the PFC of AD mice. Therapeutic interventions that manipulate sleep by targeting these pathways may be a promising approach toward delaying the progression of this incurable disease.
- Published
- 2020
49. Exploiting Common Aspects of Obesity and Alzheimer’s Disease
- Author
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Tabassum, Sidra, primary, Misrani, Afzal, additional, and Yang, Li, additional
- Published
- 2020
- Full Text
- View/download PDF
50. Microglial activation results in neuron-type-specific increase in mPFC GABAergic transmission and abnormal behavior in mice
- Author
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Tang, Binliang, primary, Jiang, Jinxiang, additional, Wang, Lei, additional, Misrani, Afzal, additional, Huo, Qingwei, additional, Han, Yuanyuan, additional, Long, Cheng, additional, and Yang, Li, additional
- Published
- 2020
- Full Text
- View/download PDF
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