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The article explores the relationship between neuroinflammatory markers, cerebrovascular injury, amyloid-beta, and Alzheimer's disease (AD) in older adults without dementia. The study found that higher plasma YKL-40 concentration was associated with greater white matter hyperintensity (WMH) volume, while higher plasma GFAP concentration was related to increased FBP SUVR. Additionally, higher plasma GFAP, WMH, and FBP SUVR were independently associated with increased pTau-217, which in turn was linked to reduced medial temporal lobe (MTL) cortical thickness and hippocampal volume, ultimately affecting memory function. The findings suggest that neuroinflammatory markers contribute to parallel pathways leading to tau-associated neurodegeneration and memory deficits in older adults, emphasizing the need for a more comprehensive approach to understanding and treating AD. [Extracted from the article]

A recent report from Oita University in Japan discusses a case of a 42-year-old man with early-onset cerebral amyloid angiopathy (CAA) and a history of childhood traumatic brain injury. The patient exhibited cognitive impairment and recurrent lobar intracerebral hemorrhaging, with brain amyloid deposition detected in specific regions. The research suggests that a single traumatic brain injury in childhood may lead to early-onset CAA, even in the absence of genetic predispositions or relevant family history. [Extracted from the article]

A recent study from George Emil Palade University of Medicine in Romania explores the roles of Clusterin and Apolipoprotein E in Alzheimer's Disease (AD) pathogenesis. Clusterin and Apolipoprotein E play significant roles in regulating amyloid-b deposition and neuronal health in AD. The study highlights the impact of the APOE4 allele on increasing the risk of late-onset AD and aims to develop targeted therapeutic approaches based on a better understanding of AD pathogenesis. [Extracted from the article]

Researchers at Tianjin University in China have developed a new approach to treating Alzheimer's disease using serum albumin-embedded copper nanoclusters. These nanoclusters demonstrated the ability to inhibit the aggregation of beta-amyloid fibrils and reduce neuroinflammation associated with the disease. The study, supported by the National Natural Science Foundation of China, showed promising results in inhibiting key pathological hallmarks of Alzheimer's disease. The findings suggest a potential new treatment strategy for this neurodegenerative condition. [Extracted from the article]

A recent study conducted by the University of California explored the association between chronic pain and Alzheimer's disease (AD)-related biomarkers in older men. The researchers found that chronic pain was related to higher levels of plasma amyloid-beta (Ab) when accompanied by elevated levels of high-sensitivity C-reactive protein (hs-CRP), a marker of systemic inflammation. Additionally, higher levels of hs-CRP and Ab were associated with smaller hippocampal volumes, which are vulnerable to neurodegeneration in AD. These findings suggest that chronic pain, when accompanied by systemic inflammation, may increase the risk of neurodegeneration in AD-vulnerable regions. [Extracted from the article]

Positrigo, a Swiss company, has received the CE Mark in Europe for its dedicated brain Positron Emission Tomography (PET) system NeuroLF. This compact imaging device assists in diagnosing and monitoring brain-related disorders such as Alzheimer's disease, brain tumors, epilepsy, and Parkinson's disease. The NeuroLF system is smaller and more affordable compared to currently available clinical hybrid PET systems, making it a significant advancement in brain PET imaging. Positrigo plans to sell its technology in Europe through partnerships with local companies. This market clearance in Europe and the US opens up commercial opportunities in other parts of the world. [Extracted from the article]

Researchers from the University of Montpellier in France have conducted a study on cerebral amyloid angiopathy (CAA), a condition often associated with Alzheimer's disease. CAA is characterized by the accumulation of amyloid in blood vessels, leading to vessel fragility and various hemorrhagic complications. The researchers presented two cases of intracranial drain-related intracerebral hemorrhage in CAA patients, suggesting that vessel fragility associated with CAA may contribute to these hemorrhagic complications. Further research is needed to understand the underlying mechanisms and implications of this association. [Extracted from the article]

A recent study conducted in Miaoli, Taiwan, explored the bioactivity of amyloid-beta (Aβ) proteins on various bio-substrates, focusing on their implications for Alzheimer's disease and cerebral amyloid angiopathy. The researchers used a dynamic mode to confirm the construction of Aβ oligomers and analyzed their hydrophobicity and morphology. The results showed that specific antibodies recognized the Aβ oligomers, and different bio-substrates influenced their binding and bioactivity. The study aims to contribute to future research on cerebral amyloid angiopathy and the development of in vitro pathogenic microenvironmental models. [Extracted from the article]

A new report from Nanjing University of Aeronautics and Astronautics in China presents fresh data on the development of an electrochemical biosensor for detecting Alzheimer's disease (AD) biomarkers. The researchers have established a competitive method using a hairpin aptamer and square wave voltammetry to detect amyloid beta 1-40 (Aβ40), a core biomarker for AD. The sensor has a low detection limit of 7.14 pg/mL and a wide dynamic range of 20 pg/mL to 200 ng/mL. This research offers a rapid, sensitive, and cost-effective method for early diagnosis of AD using point-of-care technologies. [Extracted from the article]

A recent study conducted by researchers from the University of California Irvine has found that infection with Toxoplasma gondii, a parasite commonly found in cats, can reduce the presence of amyloid beta plaques in the brains of mice with Alzheimer's disease. The study aimed to determine if there were regional differences in amyloid reduction in the brains of infected mice compared to control mice. The results showed that T. gondii infection decreased amyloid burden globally in the brain, as well as in specific regions such as the cortex and hippocampus. This research provides insight into the potential role of infections in the development and progression of Alzheimer's disease. [Extracted from the article]

A recent study conducted at the Federal University Rio de Janeiro in Brazil explores the potential of natural products in targeting the neurotoxicity of amyloid-(3 oligomers (A(3Os) in Alzheimer's disease (AD). The study highlights the critical role of A(3Os in AD pathogenesis and suggests that targeting these oligomers could be a promising therapeutic approach to mitigate cognitive decline in AD. The researchers discuss how natural products modulate A(3O neurotoxicity in various experimental systems, providing valuable insights into novel therapeutic strategies for AD. This research has been peer-reviewed and may be of interest to those studying neurodegenerative diseases and conditions. [Extracted from the article]

A recent study conducted at Brigham and Women's Hospital in Boston, Massachusetts, explored the association between anxiety and Alzheimer's disease (AD) in older adults. The study found that higher levels of anxiety were linked to more rapid cognitive decline and progression to cognitive impairment. The researchers analyzed data from older adult participants who underwent assessments of anxiety and brain imaging scans. They discovered that greater amyloid-beta (Aβ) deposition, a hallmark of AD, was significantly associated with higher levels of worry, but not with other anxiety symptoms. These findings suggest that worry may serve as an early behavioral marker and a potential target for therapeutic interventions in preclinical AD. [Extracted from the article]

A new report from Howard University discusses the phenomenon of superradiance in biological mega-networks of tryptophan (Trp) molecules, which are found in proteins. The study explores how these networks exhibit superradiant effects, where many identical quantum systems collectively absorb and emit photons at a higher rate than individual systems. The researchers found that microtubules, actin filament bundles, and amyloid fibrils all exhibit highly superradiant states, which enhance the quantum yield and stability of these structures. The findings suggest that the high quantum yield and stable superradiant states in these biological architectures may play a photoprotective role in vivo, mitigating biochemical stress and photophysical damage. [Extracted from the article]

Researchers from the University of Kentucky have conducted a study on the potential use of a small molecule p38a MAPK inhibitor, MW150, as a treatment for Alzheimer's disease (AD). The study focused on the effects of p38a inhibition in a mouse model of mixed amyloid and vascular pathologies, which more closely resembles the comorbid conditions seen in many AD patients. The results showed that MW150 reduced behavioral impairment, synaptic loss, tau phosphorylation, and improved electrophysiological parameters, suggesting that p38 inhibitors may have a role in preserving cognition in AD. Further research is needed to understand the specific neuronal pathways involved and to explore potential applications in other comorbid conditions. [Extracted from the article]

Researchers from the University of Colorado Anschutz Medical Campus have conducted a study on the relationship between plasma glial fibrillary acidic protein (GFAP), amyloid levels, and memory performance in older adults with Alzheimer's disease (AD). The study found that higher levels of plasma GFAP were associated with altered fornix microstructure, which is involved in AD-associated cholinergic pathways. Additionally, the study showed that in individuals with low plasma amyloid levels, higher GFAP levels were linked to lower verbal memory performance. These findings suggest that astrogliosis/astrocyte reactivity may play an early role in AD pathogenesis and that high GFAP and low amyloid levels may have a detrimental synergistic effect on memory pathways. [Extracted from the article]

A study conducted in Tianjin, People's Republic of China, explored the potential effects of lentinan, a natural product commonly used in medicine and dietary supplements, on Alzheimer's disease (AD) and Parkinson's disease (PD). The study found that lentinan inhibited the formation of beta-amyloid and alpha-synuclein fibers, which are associated with the pathogenesis of AD and PD, respectively. Lentinan also protected against damage caused by the accumulation of these proteins and demonstrated beneficial effects in AD and PD mice. The research suggests that lentinan may have potential therapeutic applications for neurodegenerative diseases. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the protective variant PLCgamma2-P522R and its potential role in reducing the risk of late onset Alzheimer's disease (LOAD). The study investigates the effects of this variant on microglia activation, beta-amyloid plaque burden, and neuronal pathologies in mouse models of Alzheimer's disease. The results suggest that the PLCgamma2-P522R variant may enhance microglial barrier formation around beta-amyloid plaques and suppress pro-inflammatory activation, potentially mitigating Alzheimer's disease-associated pathology. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

Auburn University researchers have found that troriluzole, a glutamate modulator, can rescue deficits in glutamatergic function, amyloid and tau pathology, and synaptic and memory impairments in a mouse model of Alzheimer's disease. The study suggests that presynaptic alterations are early events in Alzheimer's disease and could be potential targets for therapeutic intervention. Troriluzole treatment reduced glutamate release and restored cognitive deficits in the mice. These findings support the potential of glutamate-modulating drugs like troriluzole in the treatment of Alzheimer's disease. [Extracted from the article]

A recent report from Ohio State University discusses the relationship between traumatic brain injury (TBI) and Alzheimer's disease (AD). The researchers found that individuals with a history of TBI had higher levels of amyloid-beta (Aβ) peptides in their cerebrospinal fluid (CSF) compared to controls. These higher levels of Aβ peptides were associated with poorer performance on cognitive tests related to preclinical AD. The study suggests that TBI may increase the risk of AD and cognitive vulnerability through Aβ overproduction. The researchers propose that biomarker models incorporating multiple Aβ peptides could help identify AD risk in individuals with TBI. [Extracted from the article]

A recent study conducted by researchers at Emory University School of Medicine has shed light on the early regional vulnerability in Alzheimer's Disease (AD). The study found that hyperexcitability, a key factor in cognitive decline, first emerges in the entorhinal cortex. The researchers discovered that this hyperexcitability is due to the selective vulnerability of parvalbumin interneurons in the entorhinal cortex. The study suggests that early interventions targeting inhibitory neurons may protect vulnerable regions from the effects of amyloid precursor protein (APP) and tau pathology. [Extracted from the article]

A recent study conducted by researchers at the University of Melbourne highlights the development of a new cognitive composite called the Data-driven Preclinical Alzheimer's Cognitive Composite (D-PACC). This composite was designed to improve sensitivity in detecting amyloid-b status in individuals with preclinical Alzheimer's disease. The D-PACC showed comparable or improved sensitivity compared to existing composites, with higher consistency across studies. This research provides valuable insights into the development of more effective screening tools for Alzheimer's disease. [Extracted from the article]

A study examined whether plasma biomarkers can distinguish between individuals with cerebral amyloid angiopathy (CAA) and healthy controls. CAA is characterized by the deposition of beta-amyloid in small vessels, leading to hemorrhagic stroke and dementia. The study found that plasma AB42/40 ratios were significantly lower in individuals with CAA compared to healthy controls. Additionally, phosphorylated-tau and neurofilament light chain levels were elevated in CAA, while Glial Fibrillary Acidic Protein levels were similar. The combination of AB42/40, phosphorylated-tau, and neurofilament light chain biomarkers showed promise in discriminating CAA from healthy controls. However, it is important to note that this study has not yet undergone peer review. [Extracted from the article]

A recent study conducted by researchers at the University of Lisbon aimed to understand the natural history of patients with amnestic mild cognitive impairment (aMCI) who do not exhibit biomarkers of amyloid pathology or neuronal injury. The study followed 21 amyloid-negative and neurodegeneration-negative aMCI patients for an average of 7.1 years and found that they did not experience cognitive decline during the follow-up period. However, these patients did maintain persistent cognitive deficits and distressing memory complaints. The researchers concluded that adequate strategies are needed to treat this chronic clinical condition. [Extracted from the article]

A recent report from the University of Gothenburg discusses research findings on Alzheimer's disease. The study focuses on the Gothenburg Mild Cognitive Impairment (MCI) study, which examines patients seeking help for cognitive complaints. The researchers used biomarker analysis to explore preclinical cerebrospinal fluid (CSF) biomarkers for subcortical small-vessel disease (SSVD). They found that higher levels of soluble amyloid precursor proteins (sAPP-a and sAPP-b) at baseline were associated with a lower risk of converting to SSVD. These proteins could potentially be used as biomarkers to evaluate progression to SSVD. [Extracted from the article]

A recent study conducted by researchers at Brigham and Women's Hospital in Boston, Massachusetts, explored the relationship between depressive symptoms and amyloid accumulation in the brains of older adults. The study found that increasing depressive symptoms over time were associated with amyloid accumulation in brain regions related to emotional control, even in individuals who were cognitively unimpaired. These associations remained significant even after accounting for cognitive changes. The findings highlight the importance of monitoring mood symptoms early in Alzheimer's disease and provide insight into the neurobiology of depressive symptoms in older individuals. [Extracted from the article]

A recent preprint abstract discusses a new method called SynPull for studying neurodegeneration-related aggregates in synaptosomes using super-resolution microscopy. The study focuses on alpha-synuclein, beta-amyloid, and tau proteins, which are associated with Alzheimer's and Parkinson's disease. The researchers used SynPull to analyze the quantity and morphology of these aggregates in post-mortem human brain samples and mouse models. The results suggest that AT8-positive tau is the predominant aggregate type in Alzheimer's disease, while alpha-synuclein and beta-amyloid aggregates are found in smaller amounts. This method could help further understand the disease mechanisms causing synaptic dysfunction in dementia. However, it's important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A recent study conducted by researchers at the Koneru Lakshmaiah Education Foundation in Andhra Pradesh, India, explored the potential anti-Alzheimer's disease (AD) effects of indole-3 carbinol (I3C) and diindolylmethane (DIM). The study utilized docking and molecular dynamic studies, as well as network pharmacological studies, to investigate the neuroprotective effects of I3C and DIM against beta-amyloid (Ab)-induced neurotoxicity and acetylcholinesterase (AchE) enzyme activity. The results showed that both I3C and DIM exhibited anti-AD effects by inhibiting Ab-induced neurotoxicity and AchE activities. These findings suggest that I3C and DIM may have potential therapeutic applications in the treatment of AD. [Extracted from the article]

A recent study conducted by the European Brain Research Institute has found that inhibiting the colony stimulating factor 1-receptor (CSF-1R) can lead to the clearance of amyloid-beta (Ab) from glutamatergic terminals in the brain. This clearance of Ab is associated with the restoration of long-term potentiation (LTP) and excitatory transmission, which are often impaired in Alzheimer's disease (AD). The study suggests that targeting CSF-1R could be a potential disease-modifying approach for AD. The findings highlight the role of microglia, traditionally considered immune cells, in driving neuroinflammation and synaptic dysfunction in the early stages of AD. [Extracted from the article]

A new study conducted by researchers at Purdue University in West Lafayette, Indiana, focuses on cotton wool plaques (CWPs) in individuals with dominantly inherited Alzheimer's disease (DIAD). CWPs are round, eosinophilic amyloid-beta (Aβ) plaques that lack an amyloid core and are recognizable but not fluorescent in Thioflavin S preparations. The study reports the structure of Aβ and tau filaments isolated from brain tissue of individuals affected by DIAD caused by specific mutations. The findings are relevant for the development of PET imaging methodologies to detect CWPs in DIAD. [Extracted from the article]

Researchers at Nantong University in China have conducted a study on the potential benefits of Bryostatin-1, a protein kinase C (PKC) epsilon activator, in Alzheimer's disease (AD) animal models. The study found that Bryostatin-1 protected synaptic dynamics and functions against the neurotoxicity of amyloid-beta (Ab) oligomers, which are associated with AD. Additionally, Bryostatin-1 was found to rescue impaired autophagy influx caused by Ab oligomer treatment. These findings suggest that PKC epsilon activators like Bryostatin-1 could be developed as therapeutics for AD. [Extracted from the article]

A recent study conducted at Peking Union Medical College Hospital in Beijing, China, has evaluated the diagnostic value of a novel PET tracer called [18F]-Florbetazine for Alzheimer's disease (AD) and the quantification of b-amyloid (Ab) depositions in the brain. The researchers found that [18F]-Florbetazine showed high uptake on Ab plaques and provided high gray-to-white contrast in AD patients, making it potentially useful for detecting and quantifying Ab depositions in the living human brain. The study suggests that [18F]-Florbetazine could be a valuable tool for diagnosing and studying AD. [Extracted from the article]

Researchers at Dankook University in South Korea have identified bioactive compounds in the aerial parts of Agrimonia pilosa that have inhibitory effects on beta-amyloid production and aggregation. Beta-amyloid is a significant component of senile plaques and is recognized as a primary contributor to Alzheimer's disease (AD) pathology. The ethanol extract of A. pilosa reduced the levels of certain enzymes involved in beta-amyloid production and also hindered the aggregation of beta-amyloid into fibrils. The study suggests that A. pilosa extract and its active constituents hold promise for the development of therapeutics and preventatives for AD. [Extracted from the article]

A new study conducted by researchers from the National and Kapodistrian University of Athens reveals that normal pressure hydrocephalus (iNPH), a neurological syndrome characterized by cognitive deficits, gait disturbances, and urinary incontinence, often coexists with Alzheimer's disease (AD). The study aimed to determine the prevalence of beta-amyloid pathology and AD co-pathology in iNPH patients by measuring cerebrospinal fluid (CSF) biomarkers. The results showed that amyloid pathology and AD co-pathology are common in iNPH patients, and higher levels of certain CSF markers are associated with more severe memory impairment. This study confirms the link between iNPH and AD and provides valuable insights into the neuropsychological features of iNPH patients. [Extracted from the article]

A recent study conducted by researchers at the University of South Florida has explored the use of blood-based markers for diagnosing Alzheimer's disease (AD). Traditionally, AD has been identified through invasive and expensive methods such as cerebrospinal fluid analysis or positron emission tomography scans. However, recent advancements in mass spectrometry and immunoassay techniques have made it possible to detect blood markers of amyloid and tau deposition, with phosphorylated tau (p-tau) showing promise in reflecting amyloid pathology. Among the various isoforms of p-tau, p-tau217 has emerged as a reliable marker for diagnosing AD accurately and providing early prognosis. This narrative review aims to explore the utility of p-tau217 as an AD marker, including its underlying basis, clinical diagnostic potential, and relevance in clinical care and trials. [Extracted from the article]

A recent study conducted by researchers at Loma Linda University in California has shed light on type C Niemann-Pick disease (NPC), a rare and fatal neurological disorder. The study found that mutations in the Npc1 or Npc2 genes are responsible for NPC, with Npc1 accounting for 95% of cases. These mutations lead to disrupted lipid regulation, calcium dysfunction, and a pro-inflammatory environment, ultimately causing neurodegeneration. The researchers also discovered a potential role for the Amyloid Precursor Protein (APP) in NPC, as loss of APP function was found to exacerbate interferon signaling and contribute to cholesterol and tau dysregulation in the brain. This study provides valuable insights into the early pathogenic mechanisms of NPC and highlights the importance of further research in this area. [Extracted from the article]

New research from Washington University School of Medicine suggests that people with multiple sclerosis (MS) are less likely to have the molecular hallmarks of Alzheimer's disease. This discovery could provide a new avenue for Alzheimer's treatments. The study used a new blood test to confirm the observation that MS patients were not developing Alzheimer's disease. The researchers also found that the more typical the patient's MS history was, the less likely they were to have amyloid plaque accumulation in the brain, suggesting that there is something about the nature of MS itself that is protective against Alzheimer's disease. [Extracted from the article]

A recent study conducted at the University of Illinois in Urbana has explored the use of benzothiazole-based Ir(iii) complexes as inhibitors and probes of amyloid beta (Aβ) aggregation in Alzheimer's disease (AD). The researchers found that these complexes demonstrated significant inhibition of Aβ aggregation in vitro and in living cells. Additionally, the complexes exhibited enhanced blood-brain barrier permeability and successfully stained amyloid plaques in AD mouse brains, suggesting their potential as lead compounds for therapeutic and diagnostic agents in AD. The study was supported by the National Institutes of Health (NIH) in the United States. [Extracted from the article]

Researchers from Xizang Minzu University in Shaanxi, China have developed multifunctional carbon quantum dots (CQDs) that can target amyloid aggregation, overcome the blood-brain barrier (BBB), and scavenge reactive oxygen species (ROS). These CQDs, known as red emission carbon quantum dots (RCQDs), demonstrated high inhibition and disaggregation efficiencies against amyloid aggregates and showed exceptional targeting affinity for amyloid species. They also exhibited strong penetration through the BBB and displayed anti-neuroinflammation properties. This study suggests that RCQDs have therapeutic potential for the treatment of Alzheimer's disease. [Extracted from the article]

A new study conducted by researchers at the University of Murcia in Spain explores the potential of piano-stool metal complexes as inhibitors of amyloid-beta aggregation in Alzheimer's disease. The study found that these metal complexes, particularly those containing ruthenium, iridium, and rhodium, showed promising inhibitory effects on amyloid-beta aggregation in vitro. In vivo studies using a Caenorhabditis elegans animal model of Alzheimer's disease also demonstrated the potential of these complexes as inhibitors. This research provides new insights into the development of effective treatments for Alzheimer's disease. [Extracted from the article]

A recent report from the University of Strasbourg in France explores the potential neurotoxicity of monomeric amyloid peptide (ABM) in early stages of Alzheimer's disease (AD). The study investigates the effects of ABM on human oligodendrocyte cell lines and mouse brain primary mixed-glial cell cultures. The researchers found that ABM concentrations significantly decreased cell survival, with oligodendrocytes being the most vulnerable cell population. Additionally, the neurosteroid 3 alpha-O-allyl-allopregnanolone BR351 showed promise in preventing ABM-induced toxicity. The study suggests that further research on BR351's therapeutic potential could lead to effective neuroprotective strategies. [Extracted from the article]

A recent study conducted by researchers at the University of California Davis utilized machine learning to quantify amyloid-b (Ab) deposits in the temporal lobe of 131 brain bank cases. The study aimed to validate an automatic workflow for Ab deposit quantification and investigate the distribution of different Ab deposit types in gray matter (GM) and white matter (WM). The results showed a progressive increase in Ab deposits with the severity of established diagnostic criteria for Alzheimer's disease (AD). The study highlights the potential of machine learning approaches in neuropathology research and provides a foundation for further advancements in the field. [Extracted from the article]

A recent study conducted at Anhui Medical University in Hefei, China, has explored the use of a novel siRNA-based therapy for the treatment of Alzheimer's disease (AD). The researchers focused on targeting the accumulation of toxic beta-amyloid (Aβ) plaques and the expression of Ripk1, a protein associated with neuronal death in AD. They developed a nanomedicine called SH-RVG/siRipk1, which effectively reduced plaques, improved memory impairment, and rescued necrotic neurons in AD mice. These findings suggest that SH-RVG/siRipk1 could be a promising strategy for AD treatment. The research has been peer-reviewed and published in the Chemical Engineering Journal. [Extracted from the article]

A study conducted in Cantabria, Spain, examined the diagnostic accuracy of the fully-automated Lumipulse plasma p-tau217 assay in identifying preclinical Alzheimer's disease (AD) pathology. The study found that plasma p-tau217 levels correlated significantly with cerebrospinal fluid (CSF) biomarkers associated with AD. Additionally, plasma p-tau217 levels were higher in subjects with amyloid deposition in the brain, and the assay predicted CSF amyloid pathology with an area under the curve (AUC) of 0.85. The researchers concluded that plasma p-tau217 measured using the Lumipulse platform shows promise as an accurate biomarker for preclinical AD pathology. [Extracted from the article]

Researchers from Polytechnic University Milan in Italy have conducted a study on the treatment of Alzheimer's disease (AD) using Capture-Enhanced Neutron Irradiation. AD is the most common cause of dementia, affecting millions of people worldwide. The study focused on the beta amyloid peptide Aβ, which is believed to be a key factor in the development of AD. The researchers developed a new low-pressure tissue-equivalent proportional counter (TEPC) to measure the micro-nanometric dose deposition in biological samples. The results of the study provide valuable insights into the microdosimetric and nanodosimetric characterization of the secondary mixed field emitted by a biological sample irradiated with neutrons. [Extracted from the article]

New research from Southern Illinois University Edwardsville explores the role of the transmembrane protein b-amyloid precursor protein (APP) in Alzheimer's disease (AD). The study focuses on the synaptic function of APP and its relationship with Kismet (Kis), a chromatin helicase binding domain (CHD) protein. The researchers found that loss of function mutations in kis and animals expressing human APP and BACE in their central nervous system showed deficiencies in synaptic components and impaired processes like endocytosis and neurotransmission. These findings suggest a potential connection between chromatin remodeling proteins and synaptic dysfunction in AD. [Extracted from the article]

A recent study conducted by researchers at the Affiliated Hospital of Qingdao University explores the relationship between cerebrospinal fluid (CSF) sTREM2, Alzheimer's disease (AD) pathology, minimal depressive symptoms (MDSs), and cognition in non-demented adults. The study included 545 individuals from the Alzheimer's Disease Neuroimaging Initiative cohort, with an average age of 72.6 years and 42.6% female participants. The findings suggest that individuals with MDSs have lower levels of CSF sTREM2 compared to normal controls. Additionally, CSF sTREM2 may potentially serve as an intervenable target between depression and AD pathology. [Extracted from the article]

A recent study conducted by researchers at New York University (NYU) explores the differences in the proteome of cerebral amyloid angiopathy (CAA) in Alzheimer's disease (AD) and mild cognitive impairment (MCI). CAA is characterized by the deposition of amyloid beta (A beta) in the cerebrovasculature and is associated with aging and AD. The study found that there were significant differences in the abundance of proteins in CAA-positive vessels compared to neighboring CAA-negative vessels in both MCI and AD cases. These findings provide insights into the molecular mechanisms underlying CAA and its association with cognitive deficits. [Extracted from the article]

A recent report from Cornell University explores the role of monomeric and oligomeric amyloid-beta (Aβ) in astrocyte dysfunction in Alzheimer's disease (AD). The study used a brain-mimicking three-dimensional (3D) extracellular matrix to culture astrocytes and found that both monomeric and oligomeric Aβ caused astrocytic atrophy and hyper-reactivity, but with distinct calcium (Ca2+) changes. The researchers also developed a microfluidic glymphatics-on-chip model that replicated the astrocytic changes induced by Aβ and maintained the components of the dystrophin-associated complex (DAC) and aquaporin-4 (AQP4). The study concludes that monomeric and oligomeric Aβ have distinct pathophysiological effects on astrocytes in AD. [Extracted from the article]

A recent study conducted at the Catholic University of Korea explored the use of brain volumetry to predict amyloid positivity in patients with subjective cognitive decline (SCD). Amyloid beta PET screening is currently expensive and exposes patients to radiation, so the researchers sought an alternative method. They used 3D T1 MRI scans and genetic information to measure brain volume and thickness in different regions of the brain. By training machine learning models with this data, along with age and APOE4 information, the researchers were able to predict amyloid positivity in SCD patients. The study found significant differences in choroid plexus volume and lingual cortex thickness between amyloid positive and negative SCD patients. The researchers concluded that using both APOE4 information and brain volumetry is crucial for accurate amyloid positivity prediction. This study was supported by a grant from the Ministry of Health and Welfare. [Extracted from the article]

A recent study conducted by researchers at Amsterdam University Medical Center explored the potential use of digital speech assessment in the early stages of Alzheimer's disease. The study involved 50 cognitively unimpaired adults who completed remote speech assessments over a five-day period. The researchers found that the speech assessment was feasible and reliable, and they observed associations between certain speech features and amyloid-beta pathology, a hallmark of Alzheimer's disease. These findings suggest that speech biomarkers could be used in the early detection of Alzheimer's disease. [Extracted from the article]