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Anxiety disorder is one of the most well-characterized behavioral disorders in individuals subjected to acute or chronic stress. However, few studies have demonstrated how different types of stressors can modulate the neurochemical alterations involved in the generation of anxiety. In this study, we hypothesize that subjects exposed to different aversive stimuli (mechanical, chemical, and spatial restriction) present varied intensities of anxiety-like responses associated with distinct patterns of gamma-aminobutyric acid (GABA) and glutamate release in the brain. Adult zebrafish, Danio rerio (n = 60), were randomly divided into four experimental groups; control, acute restraint stress (ARS), conspecific alarm substance (CAS), and chasing with net (CN). After the stress protocols, the animals were individually transferred to a novel tank diving test for behavioral analysis. Subsequently, their brains were collected and subjected to GABA and glutamate release assay for quantification by HPLC. Our behavioral results showed that all aversive stimuli were capable of inducing anxiety-like behavior. However, the impact of anxiogenic behavior was more prominent in the CN and CAS groups when compared to ARS. This phenomenon was evident in all analyzed behavioral parameters (time on top, freezing, mean speed, maximum speed, and erratic swimming). Our data also showed that all aversive stimuli significantly decreased GABA release compared to the control group. Only animals exposed to CN and CAS presented an increase in extracellular glutamate levels. Different acute stressors induced different levels of anxiety-like behavior in zebrafish as well as specific alterations in GABAergic and glutamatergic release in the brain. These results demonstrate the complexity of anxiety disorders, highlighting that both behavioral and neurochemical responses are highly context-dependent. [ABSTRACT FROM AUTHOR]

In this article, we explore the idea that music listening can achieve neurological and psychological effects that are somewhat similar to those facilitated by psychoactive substances. To motivate this claim, we delve into the mechanisms behind music perception, psychoactive substance use, and their mutual relationship, relying on recent developments in psychedelic therapy and neuropsychopharmacology. Using a comparative approach, we discuss some underlying mechanisms of peak experiences and their neurochemical properties and suggest that music may be regarded as an alternative psychoactive trigger, prompting neurochemical responses in the brain, with resulting feelings of coping, (aesthetic) pleasure, and reward. [ABSTRACT FROM AUTHOR]

Objectives: To test the hypothesis that depressive symptoms vary with high-sensitivity C-reactive protein (hs-CRP), among older adults with obesity. Methods: This was a cross-sectional, secondary analysis of baseline data from two related lifestyle intervention trials. The study sample comprises 148 consecutively recruited, community-dwelling older adults (age >=65 years) without severe psychiatric illness and with body mass index >=30 kg/m2. Logarithmically transformed GDS was analyzed as the dependent variable. Independent variables included log-transformed hs-CRP and covariates: sex, age, and concurrent use of antidepressant medication at baseline. An additional analysis was performed using binary conversion of the GDS scores, wherein a cutoff score of 5 was considered positive for depressive symptoms. Results: Sample mean GDS score was 2.7 (SD 3.0, range 0 – 14). A significant multivariate model of GDS scores (R2 =.089, F = 3.5, P =.010) revealed log-transformed hs-CRP (P =.017) and male sex (P =.012) as associated with depressive symptoms. Supplemental analysis demonstrated associations between depressive symptoms and log-transformed hs-CRP (OR 2.17, P =.001) and between depressive symptoms and male sex (OR 3.78, P =.013). Univariate logistic regression found hs-CRP to be associated with depressive symptoms. Conclusions: In older adults with obese BMI, male sex and higher hs-CRP are associated with depression, even in a group with relatively minimal depressive symptoms. Hs-CRP may offer clinical utility as a biomarker for depression among older adults with obese BMI, even among those with non-severe psychiatric symptomatology. [ABSTRACT FROM AUTHOR]

Non‐coding RNAs (ncRNAs) are highly plastic RNA molecules that can sequester cellular proteins and other RNAs, serve as transporters of cellular cargo and provide spatiotemporal feedback to the genome. Mounting evidence indicates that ncRNAs are central to biology, and are critical for neuronal development, metabolism and intra‐ and intercellular communication in the brain. Their plasticity arises from state‐dependent dynamic structure states that can be influenced by cell type and subcellular environment, which can subsequently enable the same ncRNA with discrete functions in different contexts. Here, we highlight different classes of brain‐enriched ncRNAs, including microRNA, long non‐coding RNA and other enigmatic ncRNAs, that are functionally important for both learning and memory and adaptive immunity, and describe how they may promote cross‐talk between these two evolutionarily ancient biological systems. [ABSTRACT FROM AUTHOR]

Gastropod molluscs such as Aplysia, Lymnaea, and Tritonia have been important for determining fundamental rules of motor control, learning, and memory because of their large, individually identifiable neurons. Yet only a small number of gastropod neurons have known molecular markers, limiting the ability to establish brain‐wide structure–function relations. Here we combine high‐throughput, single‐cell RNA sequencing with in situ hybridization chain reaction in the nudibranch Berghia stephanieae to identify and visualize the expression of markers for cell types. Broad neuronal classes were characterized by genes associated with neurotransmitters, like acetylcholine, glutamate, serotonin, and GABA, as well as neuropeptides. These classes were subdivided by other genes including transcriptional regulators and unannotated genes. Marker genes expressed by neurons and glia formed discrete, previously unrecognized regions within and between ganglia. This study provides the foundation for understanding the fundamental cellular organization of gastropod nervous systems. [ABSTRACT FROM AUTHOR]

Anxiety disorder is one of the most well-characterized behavioral disorders in individuals subjected to acute or chronic stress. However, few studies have demonstrated how different types of stressors can modulate the neurochemical alterations involved in the generation of anxiety. In this study, we hypothesize that subjects exposed to different aversive stimuli (mechanical, chemical, and spatial restriction) present varied intensities of anxiety-like responses associated with distinct patterns of gamma-aminobutyric acid (GABA) and glutamate release in the brain. Adult zebrafish, Danio rerio (n = 60), were randomly divided into four experimental groups; control, acute restraint stress (ARS), conspecific alarm substance (CAS), and chasing with net (CN). After the stress protocols, the animals were individually transferred to a novel tank diving test for behavioral analysis. Subsequently, their brains were collected and subjected to GABA and glutamate release assay for quantification by HPLC. Our behavioral results showed that all aversive stimuli were capable of inducing anxiety-like behavior. However, the impact of anxiogenic behavior was more prominent in the CN and CAS groups when compared to ARS. This phenomenon was evident in all analyzed behavioral parameters (time on top, freezing, mean speed, maximum speed, and erratic swimming). Our data also showed that all aversive stimuli significantly decreased GABA release compared to the control group. Only animals exposed to CN and CAS presented an increase in extracellular glutamate levels. Different acute stressors induced different levels of anxiety-like behavior in zebrafish as well as specific alterations in GABAergic and glutamatergic release in the brain. These results demonstrate the complexity of anxiety disorders, highlighting that both behavioral and neurochemical responses are highly context-dependent.

The article in the Journal of Neurology highlights the life and contributions of American biochemist Morris H. Aprison, who co-discovered the role of glycine as a neurotransmitter. Aprison's research also focused on the neurochemical correlates of behavior, the excitatory action of aspartate and glutamate, and molecular mechanisms of transmitter-receptor interactions. His work laid the foundation for understanding neurotransmission and its impact on behavior, earning him recognition in the field of neurochemistry. [Extracted from the article]

This preface introduces the Journal of Neurochemistry Special Issue on pain research. While acute pain provides important sensory information, which aids in the protection of an organism, it can in some cases transition into a chronic state. Unfortunately, chronic pain is a highly disabling state characterised by intense and abnormal pain sensations, which are exacerbated by problematic psychosocial disturbances that are poorly treated by current drugs. This issue includes several reviews that address current issues spanning basic to clinical research on a range of pain syndromes. Also included is a collection of basic research articles investigating important aspects of pain signalling through to whole body aspects of pain integration. [ABSTRACT FROM AUTHOR]

With sadness, the International Society for Neurochemistry (ISN) and the Journal of Neurochemistry (JNC) mourn the loss of one of the founding members of the neurochemistry field of science. Abel Lajtha, born in Budapest, Hungary on September 22, 1922, died on May 25, 2024. Abel had a long and distinguished record of service with ISN, having been a founding member of the Society, and served on the editorial board of the Society's journal, JNC. [ABSTRACT FROM AUTHOR]

The article titled "Correction to 'Wild-type Shadoo proteins convert to amyloid-like forms under native conditions'" in the Journal of Neurochemistry provides a correction to the original publication. The original gel photographs for the expression of mouse Sho25-122 could not be located, so Figure S1 panels b-e and the associated experimental methods have been deleted. New data has been added for the expression of the mouse Sho25-122 plasmid, placed in a revised Figure S2. The revised figures and legends are provided in the article. [Extracted from the article]

ObjectivesMethodsResultsDiscussionCommon mental disorders (CMD) are associated with impaired frontal excitatory/inhibitory (E/I) balance and reduced grey matter volume (GMV). Larger GMV (in the areas that are implicated in CMD-pathology) and improved CMD-symptomatology have been observed in individuals who adhere to high quality diets. Moreover, preclinical studies have shown altered neurometabolites (primarily gamma-aminobutyric acid: GABA and glutamate: GLU) in relation to diet quality. However, neurochemical correlates of diet quality and how these neurobiological changes are associated with CMD and with its transdiagnostic factor, rumination, is unknown in humans. Therefore, in this study, we examined the associations between diet quality and frontal cortex neuro-chemistry and structure, as well as CMD and rumination in humans.Thirty adults were classified into high and low diet quality groups and underwent 1H-MRS to measure medial prefrontal cortex (mPFC) metabolite concentrations and volumetric imaging to measure GMV.Low (vs High) diet quality group had reduced mPFC-GABA and elevated mPFC-GLU concentrations, as well as reduced right precentral gyrus (rPCG) GMV. However, CMD and rumination were not associated with diet quality. Notably, we observed a significant negative correlation between rumination and rPCG-GMV and a marginally significant association between rumination and mPFC-GLU concentrations. There was also a marginally significant association between mPFC-GLU concentrations and rPCG-GMV.Adhering to unhealthy dietary patterns may be associated with compromised E/I balance, and this could affect GMV, and subsequently, rumination. [ABSTRACT FROM AUTHOR]

On the surface, fear and humor seem like polar opposite states of mind, yet throughout our lives they continually interact. In this paper, we synthesize neurobiological, psychological, and evolutionary research on fear and humor, arguing that the two are deeply connected. The evolutionary origins of humor reside in play, a medium through which animals benignly explore situations and practice strategies, such as fight or flight, which would normally be accompanied by fear. Cognitively, humor retains the structure of play. Adopting a view of humor as requiring two appraisals, a violation appraisal and a benign appraisal, we describe how fear-inducing stimuli can be rendered benignly humorous through contextual cues, psychological distance, reframing, and cognitive reappraisal. The antagonistic relationship between humor and fear in terms of their neurochemistry and physiological effects in turn makes humor ideal for managing fear in many circumstances. We review five real-world examples of humor and fear intersecting, presenting new data in support of our account along the way. Finally, we discuss the possible therapeutic relevance of the deep connection between humor and fear. [ABSTRACT FROM AUTHOR]

Purpose/aim of the study: The study aimed to highlight the possible role of ciliary neurotrophic factor (CNTF) in the pathophysiology of attention deficit hyperactivity disorder (ADHD) and determine whether CNTF can be used as a biomarker for ADHD.Materials and methods: Patients with a diagnosis of ADHD and neurotypical subjects aged 6–12 years were recruited prospectively. The study applied Conners' Teacher Rating Scale (CTRS) to determine the patients' ADHD predominance and severity. Serum CNTF levels were measured with an enzyme-linked immunosorbent assay (ELISA) kit.Results: A total of 43 ADHD patients and 33 healthy controls were included in the study. A significant difference was found between the serum CNTF levels of the ADHD patients (22.17 pg/ml) and the controls (22.80 pg/ml). Correlations between the CNTF levels and CTRS scores were not significant.Conclusions: The study identified an alteration of serum CNTF levels in ADHD patients and thus asserted a link between CNTF and ADHD pathophysiology; children with ADHD had significantly lower serum CNTF levels compared to the neurotypical controls. Further research is needed to understand the mechanisms of CNTF. [ABSTRACT FROM AUTHOR]

This preface introduces the Journal of Neurochemistry special issue on Cholinergic Mechanisms that highlights the progress in the molecular, structural, neurochemical, pharmacological, toxicological, and clinical studies of the cholinergic system which underline its complexity and impact on health and disease. This issue comprises of (systematic) reviews and original articles, the majority of which have been presented at the 17th International Symposium on Cholinergic Mechanisms (ISCM2022) held in Dubrovnik, Croatia in May 2022. The symposium brought together leading "Cholinergikers" to shed new light on cholinergic transmission, ranging from the molecular to the clinical and cognitive mechanisms. [ABSTRACT FROM AUTHOR]

Increased knowledge about sex differences is important for development of individualized treatments against many diseases as well as understanding behavioral and pathological differences. This review summarizes sex chromosome effects on gene expression, epigenetics, and hormones in relation to the brain. We explore neuroanatomy, neurochemistry, cognition, and brain pathology aiming to explain the current state of the art. While some domains exhibit strong differences, others reveal subtle differences whose overall significance warrants clarification. We hope that the current review increases awareness and serves as a basis for the planning of future studies that consider both sexes equally regarding similarities and differences. [ABSTRACT FROM AUTHOR]

Recent data suggest that 3,4-methylenedioxypyrovalerone (MDPV) has neurotoxic effects; however, the cognitive and neurochemical consequences of MDPV self-administration remain largely unexplored. Furthermore, despite the fact that drug preparations that contain MDPV often also contain caffeine, little is known regarding the toxic effects produced by the co-use of these two stimulants. The current study investigated the degree to which self-administered MDPV or a mixture of MDPV+caffeine can produce deficits in recognition memory and alter neurochemistry relative to prototypical stimulants. Male Sprague Dawley rats were provided 90 min or 12 h access to MDPV, MDPV+caffeine, methamphetamine, cocaine, or saline for 6 weeks. Novel object recognition (NOR) memory was evaluated prior to any drug self-administration history and 3 weeks after the final self-administration session. Rats that had 12 h access to methamphetamine and those that had 90 min or 12 h access to MDPV+caffeine exhibited significant deficits in NOR, whereas no significant deficits were observed in rats that self-administered cocaine or MDPV. Striatal monoamine levels were not systematically affected. These data demonstrate synergism between MDPV and caffeine with regard to producing recognition memory deficits, highlighting the importance of recapitulating the manner in which drugs are used (e.g., in mixtures containing multiple stimulants, binge-like patterns of intake). [ABSTRACT FROM AUTHOR]

Dr. Brian Collier, the former Editor‐in‐Chief of the Journal of Neurochemistry from 1996 to 2006, passed away January 4th, 2024. Brian's illustrious career spanned the fields of neurochemistry and pharmacology. He published his findings on mechanisms of acetylcholine synthesis and storage in the Journal of Neurochemistry, and his contributions remain landmarks in neurochemical research. [ABSTRACT FROM AUTHOR]

Synaptic transmission via neurochemical release is the fundamental process that integrates and relays encoded information in the brain to regulate physiological function, cognition, and emotion. To unravel the biochemical, biophysical, and computational mechanisms of signal processing, one needs to precisely measure the neurochemical release dynamics with molecular and cell-type specificity and high resolution. Here we reviewed the development of analytical, electrochemical, and fluorescence imaging approaches to detect neurotransmitter and neuromodulator release. We discussed the advantages and practicality in implementation of each technology for ease-of-use, flexibility for multimodal studies, and challenges for future optimization. We hope this review will provide a versatile guide for tool engineering and applications for recording neurochemical release.

Dapoxetine is a newer anti‐depressant that is used for severe forms of depression via selective serotonin reuptake inhibition conduit. We aimed to evaluate the effect of different doses of dapoxetine lonely or with acetaminophen (AMP). Seven groups of albino rats were used where dapoxetine was administered orally at the doses of 3, 5, and 8 mg/kg body weight for a period of 14 days in groups 2, 4, and 6, respectively. AMP (67.5 mg/kg body weight) was co‐administered with dapoxetine (3, 5, and 8 mg/kg body weight) for 14 days in groups 3, 5 and 7, respectively. Dapoxetine in mid and high dose plus AMP increased body weight and hematological parameters. Ambulation and rearing were declined with mid and high doses of dapoxetine+AMP, contrary to grooming. Struggling was decreased with high doses of dapoxetine+AMP. High dose of dapoxetine+AMP induced lowering of serotonin and dopamine as well as increasing of cholinesterase. Brain derived neurotrophic factor was decreased in all groups. Oxidative stress biomarkers were augmented with high dose of dapoxetine+AMP. High doses of dapoxetine and/or AMP induced loss of the Purkinje cell layer at cerebellum. The high dose of dapoxetine+AMP denotes behavioral, histopathological and neurochemical alterations, even though no serotonin syndrome occurs. [ABSTRACT FROM AUTHOR]

Schizophrenia is a leading cause of global disability. Current pharmacotherapy for the disease predominantly uses one mechanism — dopamine D2 receptor blockade — but often shows limited efficacy and poor tolerability. These limitations highlight the need to better understand the aetiology of the disease to aid the development of alternative therapeutic approaches. Here, we review the latest meta-analyses and other findings on the neurobiology of prodromal, first-episode and chronic schizophrenia, and the link to psychotic symptoms, focusing on imaging evidence from people with the disorder. This evidence demonstrates regionally specific neurotransmitter alterations, including higher glutamate and dopamine measures in the basal ganglia, and lower glutamate, dopamine and γ-aminobutyric acid (GABA) levels in cortical regions, particularly the frontal cortex, relative to healthy individuals. We consider how dysfunction in cortico-thalamo-striatal–midbrain circuits might alter brain information processing to underlie psychotic symptoms. Finally, we discuss the implications of these findings for developing new, mechanistically based treatments and precision medicine for psychotic symptoms, as well as negative and cognitive symptoms. Schizophrenia is a leading cause of global disability but lacks therapies that target all aspects of the disease. This Review summarizes our current understanding of the pathophysiological mechanisms underlying the disease, highlighting potential targets for new drug development. [ABSTRACT FROM AUTHOR]

While visceral pain is commonly associated with disorders of the gut–brain axis, underlying mechanisms are not fully understood. Dorsal root ganglion (DRG) neurons innervate visceral structures and undergo hypersensitization in inflammatory models. The characterization of peripheral DRG neuron terminals is an active area of research, but recent work suggests that they communicate with enteroendocrine cells (EECs) in the gut. EECs sense stimuli in the intestinal lumen and communicate information to the brain through hormonal and electrical signaling. In that context, EECs are a target for developing therapeutics to treat visceral pain. Linaclotide is an FDA‐approved treatment for chronic constipation that activates the intestinal membrane receptor guanylyl cyclase C (GUCY2C). Clinical trials revealed that linaclotide relieves both constipation and visceral pain. We recently demonstrated that the analgesic effect of linaclotide reflects the overexpression of GUCY2C on neuropod cells, a specialized subtype of EECs. While this brings some clarity to the relationship between linaclotide and visceral analgesia, questions remain about the intracellular signaling mechanisms and neurotransmitters mediating this communication. In this Fundamental Neurochemistry Review, we discuss what is currently known about visceral nociceptors, enteroendocrine cells, and the gut‐brain axis, and ongoing areas of research regarding that axis and visceral pain. [ABSTRACT FROM AUTHOR]

Personality traits play a crucial role in studying mental disorders because they offer insights into the individual differences and vulnerabilities that influence the onset, course, and treatment of these disorders. Recognizing the significance of personality in mental health research and clinical practice contributes to a more holistic and personalized approach to understanding and managing mental health conditions. Studying the relationship between personality traits and mental disorders can shed light on the underlying mechanisms and etiology of these disorders. It can help researchers identify common genetic, neural, and environmental factors that contribute to both personality traits and mental health conditions. Zebrafish are increasingly used as models for studying various mental disorders, such as anxiety, depression, and autism spectrum disorders. The existence of zebrafish personality traits can help elucidate how different individuals within a population may be more or less susceptible to these conditions. By examining the genetic underpinnings of zebrafish personality traits and their link to mental disorders, researchers can identify potential genetic markers and pathways involved in the pathogenesis of these conditions. Zebrafish research allows for in-depth exploration of the neural and neurochemical mechanisms underpinning personality traits and how these relate to mental disorders. Insights from zebrafish studies can inform our understanding of these mechanisms in more complex organisms. [ABSTRACT FROM AUTHOR]

This article is an editorial published in Frontiers in Molecular Neuroscience, discussing the legacy of Dr. Ricardo Tapia, a prominent Mexican scientist in the field of neurochemistry. Dr. Tapia had a long and successful career, publishing numerous scientific articles and mentoring many students. The editorial highlights the research areas explored by Dr. Tapia's students, including neurodegenerative diseases, spinal cord damage, ischemia, and amyotrophic lateral sclerosis. The article also mentions specific research papers within this special topic that cover various themes related to neurochemistry. [Extracted from the article]

Hermona Soreq holds a Hebrew University Slesinger Chair in Molecular Neuroscience and is among the founding members of the Edmond and Lily Safra Center of Brain Sciences (ELSC). Soreq's research (H‐impact: 98) focuses on acetylcholine (ACh)‐related pathways and combines RNA‐sequencing technologies, transgenic engineering, and molecular biology tests with in‐depth analysis approaches. Her work addresses microRNAs (miRs) and transfer RNA fragments (tRFs) which have rapidly acquired wide recognition as global controllers of regulatory processes in healthy and diseased brain and body, including anxiety, inflammation, and cognition. Altogether, Soreq's work leads to molecular neuroscience‐driven prevention and/or intervention with diseases involving impaired ACh signaling, including schizophrenia, bipolar disorder, Alzheimer's disease, and stress. Hermona led this Special Issue based on the 17th Symposium on Cholinergic Mechanisms (ISCM2022). We interviewed her on the progress in the field, what she wants to achieve as Senior Editor for the Gene Regulation and Genetics category at the Journal of Neurochemistry, key moments, and future directions. [ABSTRACT FROM AUTHOR]

Background: Psychological stress (PS) disrupts the gut microbiome, accelerates cognitive decline, and causes a predisposition to certain neurodegenerative diseases. This study was designed to test the hypothesis that the administration of probiotics has beneficial effects on the neurohistology and neurochemistry of the hippocampus following exposure to psychological stress (PS). Methods: Thirty-five adult male Wistar rats weighing 180±5g were randomly assigned to seven groups (n=5) comprising the control, acute PS, acute probiotic treatment (probio), acute PS+probio, chronic PS, chronic probio, and chronic PS+probio groups. Acute stress and chronic PS or probio treatment lasted seven and 14 days, respectively. Each animal in the probio groups was fed 10×106 colony-forming units of lactobacillus acidophilus every other day. In contrast, the PS groups were exposed to predator stress for one hour between 7-10 am daily. The treatments lasted for 14 days. Following euthanasia, blood and hippocampal samples were collected for histology, and ELISA-based assays of interleukin-1β (1IL-1β), Tumor Necrosis Factor-α (TNF-α), dopamine, serotonin, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH). Results: Data analysis reveals that acute and chronic psychological stress significantly depresses hippocampal serotonin and dopamine levels, induces the overexpression of IL-1β and TNF-α, and causes increased lipid peroxidation and impaired antioxidant parameters. The probiotics groups exhibited statistically better results on all parameters assessed, including bringing hippocampal IL-1β and TNF-α levels toward normal. No obvious histoarchitectural damages were observed in any group. Conclusion: Overall, this study suggests that the gut microbiome might play a significant role in hippocampal function as supplementing it mitigates stress-induced perturbations of hippocampal neurochemistry and redox status. Background: Psychological stress (PS) disrupts the gut microbiome, accelerates cognitive decline, and causes a predisposition to certain neurodegenerative diseases. This study was designed to test the hypothesis that the administration of probiotics has beneficial effects on the neurohistology and neurochemistry of the hippocampus following exposure to psychological stress (PS). Methods: Thirty-five adult male Wistar rats weighing 180±5g were randomly assigned to seven groups (n=5) comprising the control, acute PS, acute probiotic treatment (probio), acute PS+probio, chronic PS, chronic probio, and chronic PS+probio groups. Acute stress and chronic PS or probio treatment lasted seven and 14 days, respectively. Each animal in the probio groups was fed 10×106 colony-forming units of lactobacillus acidophilus every other day. In contrast, the PS groups were exposed to predator stress for one hour between 7-10 am daily. The treatments lasted for 14 days. Following euthanasia, blood and hippocampal samples were collected for histology, and ELISA-based assays of interleukin-1β (1IL-1β), Tumor Necrosis Factor-α (TNF-α), dopamine, serotonin, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH). Results: Data analysis reveals that acute and chronic psychological stress significantly depresses hippocampal serotonin and dopamine levels, induces the overexpression of IL-1β and TNF-α, and causes increased lipid peroxidation and impaired antioxidant parameters. The probiotics groups exhibited statistically better results on all parameters assessed, including bringing hippocampal IL-1β and TNF-α levels toward normal. No obvious histoarchitectural damages were observed in any group. Conclusion: Overall, this study suggests that the gut microbiome might play a significant role in hippocampal function as supplementing it mitigates stress-induced perturbations of hippocampal neurochemistry and redox status.

Increased knowledge about sex differences is important for development of individualized treatments against many diseases as well as understanding behavioral and pathological differences. This review summarizes sex chromosome effects on gene expression, epigenetics, and hormones in relation to the brain. We explore neuroanatomy, neurochemistry, cognition, and brain pathology aiming to explain the current state of the art. While some domains exhibit strong differences, others reveal subtle differences whose overall significance warrants clarification. We hope that the current review increases awareness and serves as a basis for the planning of future studies that consider both sexes equally regarding similarities and differences.

According to previous research, individuals with autism spectrum disorder (ASD) have lower levels of physical activity than their typically developed (TD) counterparts. There have been conflicting reports about physical activity (PA) levels in people with ASD. Given the conflicting evidence, further investigation is required. We believe that evaluating PA in individuals with ASD is critical in order to offer PA intervention plans aiming at increasing their health-related physical fitness on a daily, systematic, and individualized basis. In the current study, an ActiGraph monitor (GT3X+) was used to accurately measure PA and sedentary activity in 21 children with autism aged 6.43 ± 2.29 years and 30 TD children aged 7.2 ± 3.14 years. Our data indicated that while the light and moderate activity counts were not significantly different between the two groups, the vigorous activity was significantly higher in ASD compared to TD. This finding was attributed to ASD characteristic stereotypy and self-stimulating behaviors. The significantly higher vigorous PA is discussed in relation to altered neurochemistry, oxidative stress, and neuroinflammation as etiological mechanisms in ASD. This research provides a better understanding of the status of PA participation in individuals with ASD. [ABSTRACT FROM AUTHOR]

Immunotherapy with interferon-α (IFN-α) is frequently associated with neuropsychiatric consequences, including depression. Mechanisms underlying adverse effects of IFN-α are not fully understood. This study was aimed to determine whether intranasal administration of IFN-α can provoke depression-like behavior in rats and whether overcrowding stress can interfere or amplify the effects of IFN-α. To achieve this aim, effects of human IFN-α in low (50 IU/kg) and medium (8000 IU/kg) doses on the forced swimming test behavior and monoamines and their metabolite content in the brain structures of Wistar rats housed in standard and overcrowding conditions were investigated. Depressive-like behavior (increased immobility) was observed in rats housed in standard conditions after treatment with both doses of human IFN-α, as well as in vehicle-treated rats housed in stressful, overcrowding conditions. In standard conditions, a low dose of IFN-α produced a subtle alteration in the metabolism of dopamine only in one of the brain structures analyzed (nucleus accumbens). The medium dose of IFN-α induced more drastic neurochemical alterations in a larger number of brain structures. Overcrowding led to some changes in monoamine and their metabolite levels similar to those observed after IFN-α treatment with the medium dose in the standard housing conditions. In the overcrowded conditions, in contrast to the standard ones, IFN-α treatment in both doses reduced depression-like behavior and normalized neurochemical alterations induced by overcrowding. The results suggest that the effect of IFN-α on depression-like behavior and brain neurochemistry depends on the ongoing emotional status of animals: whether they are in stressful (overcrowded) or non-stressful (normal) conditions. [ABSTRACT FROM AUTHOR]

Mutations in the FBXO28 gene, which encodes FBXO28, one of the F-box protein family, may cause developmental and epileptic encephalopathy (DEE). FBXO28 -related DEE is radiologically characterized by cerebral atrophy, delayed/abnormal myelination, and brain malformation; however, no neurochemical analyses have been reported. Case report: A female Japanese infant presented with severe psychomotor delay, epileptic spasms, and visual impairment. Whole-exome sequencing revealed a de novo variant of the FBXO28 gene, leading to the diagnosis of FBXO28 -related DEE. Magnetic resonance (MR) spectroscopy at 6, 12, and 32 months revealed decreased N -acetylaspartate and choline-containing compounds and increased levels of myoinositol. MR spectroscopy revealed neurochemical derangement in FBXO28 -related DEE, that is, disturbed myelination secondary to neuronal damage with astrogliosis. [ABSTRACT FROM AUTHOR]

Gestational protein intake restriction-induced long-lasting harmful outcomes in the offspring's organs and systems. However, few studies have focused on this event's impact on the brain's structures and neurochemical compounds. The present study investigated the effects on the amygdala neurochemical composition and neuronal structure in gestational protein-restricted male rats' offspring. Dams were maintained on isocaloric standard rodent laboratory chow with regular protein [NP, 17%] or low protein content [LP, 6%]. Total cells were quantified using the Isotropic fractionator method, Neuronal 3D reconstruction, and dendritic tree analysis using the Golgi–Cox technique. Western blot and high-performance liquid chromatography performed neurochemical studies. The gestational low-protein feeding offspring showed a significant decrease in birth weight up to day 14, associated with unaltered brain weight in youth or adult progenies. The amygdala cell numbers were unchanged, and the dendrites length and dendritic ramifications 3D analysis in LP compared to age-matched NP progeny. However, the current study shows reduced amygdala content of norepinephrine, epinephrine, and dopamine in LP progeny. These offspring observed a significant reduction in the amygdala glucocorticoid (GR) and mineralocorticoid (MR) receptor protein levels. Also corticotrophin-releasing factor (CRF) amygdala protein content was reduced in 7 and 14-day-old LP rats. The observed amygdala neurochemical changes may represent adaptation during embryonic development in response to elevated fetal exposure to maternal corticosteroid levels. In this way, gestational malnutrition stress can alter the amygdala's neurochemical content and may contribute to known behavioral changes induced by gestational protein restriction. [ABSTRACT FROM AUTHOR]

Our brains have a propensity to integrate closely-timed auditory and visual stimuli into a unified percept; a phenomenon that is highly malleable based on prior sensory experiences, and is known to be altered in clinical populations. While the neural correlates of audiovisual temporal perception have been investigated using neuroimaging and electroencephalography techniques in humans, animal research will be required to uncover the underlying cellular and molecular mechanisms. Prior to conducting such mechanistic studies, it is important to first confirm the translational potential of any prospective animal model. Thus, in the present study, we conducted a series of experiments to determine if rats show the hallmarks of audiovisual temporal perception observed in neurotypical humans, and whether the rat behavioral paradigms could reveal when they experienced perceptual disruptions akin to those observed in neurodevelopmental disorders. After training rats to perform a temporal order judgment (TOJ) or synchrony judgment (SJ) task, we found that the rats' perception was malleable based on their past and present sensory experiences. More specifically, passive exposure to asynchronous audiovisual stimulation in the minutes prior to behavioral testing caused the rats' perception to predictably shift in the direction of the leading stimulus; findings which represent the first time that this form of audiovisual perceptual malleability has been reported in non-human subjects. Furthermore, rats performing the TOJ task also showed evidence of rapid recalibration, in which their audiovisual temporal perception on the current trial was predictably influenced by the timing lag between the auditory and visual stimuli in the preceding trial. Finally, by manipulating either experimental testing parameters or altering the rats' neurochemistry with a systemic injection of MK-801, we showed that the TOJ and SJ tasks could identify when the rats had difficulty judging the timing of audiovisual stimuli. These findings confirm that the behavioral paradigms are indeed suitable for future testing of rats with perceptual disruptions in audiovisual processing. Overall, our collective results highlight that rats represent an excellent animal model to study the cellular and molecular mechanisms underlying the acuity and malleability of audiovisual temporal perception, as they showcase the perceptual hallmarks commonly observed in humans. [ABSTRACT FROM AUTHOR]

Background: Despite observed sex differences in the prevalence of stress-related psychiatric conditions, most preclinical and translational studies have only included male subjects. Therefore, it has not been possible to effectively assess how sex interacts with other psychosocial risk factors to impact the etiology and maintenance of stress-related psychopathology. One psychosocial factor that interacts with sex to impact risk for stress-related behavioral and physiological deficits is social dominance. The current study was designed to assess sex differences in the effects of social status on socioemotional behavior and serotonin neurochemistry in socially housed rhesus monkeys. We hypothesized that sex and social status interact to influence socioemotional behaviors as well as serotonin 1A receptor binding potential (5HT1AR-BP) in regions of interest (ROIs) implicated in socioemotional behavior. Methods: Behavioral observations were conducted in gonadally intact adult female (n = 14) and male (n = 13) rhesus monkeys. 5HT1AR-BP was assessed via positron emission tomography using 4-(2ʹ-Methoxyphenyl)-1-[2ʹ-(N-2ʺ-pyridinyl)-p[18F]fluorobenzamido]ethylpiperazine ([18F]MPPF). Results: Aggression emitted was greater in dominant compared to subordinate animals, regardless of sex. Submission emitted was significantly greater in subordinate versus dominant animals and greater in females than males. Affiliative behaviors emitted were not impacted by sex, status, or their interaction. Anxiety-like behavior emitted was significantly greater in females than in males regardless of social status. Hypothalamic 5HT1AR-BP was significantly greater in females than in males, regardless of social status. 5HT1AR-BP in the dentate gyrus of the hippocampus was significantly impacted by a sex by status interaction whereby 5HT1AR-BP in the dentate gyrus was greater in dominant compared to subordinate females but was not different between dominant and subordinate males. There were no effects of sex, status, or their interaction on 5HT1AR-BP in the DRN and in the regions of the PFC studied. Conclusions: These data have important implications for the treatment of stress-related behavioral health outcomes, as they suggest that sex and social status are important factors to consider in the context of serotonergic drug efficacy. Plain language summary: Females are more likely to suffer from stress-related conditions that impact socioemotional behavior compared to males. One thing that influences how sex impacts stress-related health problems is social dominance. We examined whether there are sex differences in the effects of social dominance on socioemotional behavior in socially housed rhesus monkeys. Because the neurotransmitter serotonin is important for socioemotional behavior, we also looked at the levels of the 5HT1AR receptor using neuroimaging. Aggression was greater in dominant compared to subordinate animals, and submission was significantly greater in subordinate versus dominant animals and greater in females than males. Anxiety and levels of 5HT1AR in the hypothalamus were significantly greater in females than in males. 5HT1AR in the hippocampus was greater in dominant compared to subordinate females but was not different between dominant and subordinate males. Overall, these data are important for the treatment of stress-related behavioral health outcomes because suggest that sex and social dominance are important factors to consider in the context of how effective drugs targeting the serotonin system are for treating stress-related behavioral health conditions. Highlights: Investigation of sex and social status impacts risk on socioemotional and serotonin 5HT1A receptor binding potential (5HT1AR-BP) in rhesus monkeys. Aggression emitted was greater in dominant compared to subordinate animals, and submission emitted was significantly greater in subordinate versus dominant animals and greater in females than males. Anxiety-like behavior and hypothalamic 5HT1AR-BP were significantly greater in females than in males. 5HT1AR-BP in the dentate gyrus was greater in dominant compared to subordinate females but was not different between dominant and subordinate males. These data have important implications for the treatment of stress-related behavioral health outcomes. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain‐infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro‐ and anti‐inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro‐inflammatory activation is associated with decreased mitochondrial respiration, whereas anti‐inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post‐traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non‐resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post‐traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI. [ABSTRACT FROM AUTHOR]

This study examined the molecular underpinnings of group instrumental music improvisation as well as verbal improvisation in musicians and nonmusicians using blood-based measurements of oxytocin, vasopressin, dopamine, and cortisol, with verbal improvisation serving as a control. All participants (N = 8) were able to successfully complete study tasks as directed and tolerate the blood draws. On average, regardless of musicianship status, males had a greater and directionally divergent change in cortisol when compared to females (males M = -.033; females M = .025) after improvising musically (p < .04). Males also had a significant difference between the decrease in cortisol after music improvisation (M = -.033) compared to an increase in cortisol after verbal improvisation (M = .026; p < .01). The current investigation provided promising results regarding the ability of the study design and procedures to yield useful information when bringing the study to scale with a sufficiently powered sample indicating potential sex and modality based differences. [ABSTRACT FROM AUTHOR]

Objective: Spinocerebellar ataxia type 3 (SCA3) is the most common dominantly inherited ataxia, and biomarkers are needed to noninvasively monitor disease progression and treatment response. Anti‐ATXN3 antisense oligonucleotide (ASO) treatment has been shown to mitigate neuropathology and rescue motor phenotypes in SCA3 mice. Here, we investigated whether repeated ASO administration reverses brainstem and cerebellar neurochemical abnormalities by magnetic resonance spectroscopy (MRS). Methods: Symptomatic SCA3 mice received intracerebroventricular treatment of ASO or vehicle and were compared to wild‐type vehicle‐treated littermates. To quantify neurochemical changes in treated mice, longitudinal 9.4T MRS of cerebellum and brainstem was performed. Acquired magnetic resonance (MR) group means were analyzed by 2‐way analysis of variance mixed‐effects sex‐adjusted analysis with post hoc Sidak correlation for multiple comparisons. Pearson correlations were used to relate SCA3 pathology and behavior. Results: MR spectra yielded 15 to 16 neurochemical concentrations in the cerebellum and brainstem. ASO treatment in SCA3 mice resulted in significant total choline rescue and partial reversals of taurine, glutamine, and total N‐acetylaspartate across both regions. Some ASO‐rescued neurochemicals correlated with reduction in diseased protein and nuclear ATXN3 accumulation. ASO‐corrected motor activity correlated with total choline and total N‐acetylaspartate levels early in disease. Interpretation: SCA3 mouse cerebellar and brainstem neurochemical trends parallel those in patients with SCA3. Decreased total choline may reflect oligodendrocyte abnormalities, decreased total N‐acetylaspartate highlights neuronal health disturbances, and high glutamine may indicate gliosis. ASO treatment fully or partially reversed select neurochemical abnormalities in SCA3 mice, indicating the potential for these measures to serve as noninvasive treatment biomarkers in future SCA3 gene silencing trials. ANN NEUROL 2023;94:658–671 [ABSTRACT FROM AUTHOR]

In considering the hopeful rhetoric that pervades the "nothing but" psychopharmacological approaches to depression—a contemporary version of what William James calls medical materialism—this article argues that only a thorough-going pluralist account of hope is a hope worth wanting. Medical materialist hope is better conceptualized as a variation of optimism, which assumes a single universe that is already the best of all possible universes, and thereby only promotes optimization of the status quo, rather than encourage a wider undertaking of a variety of experiments in living. A pluralist hope, as opposed to optimism, cannot logically infer what the future will bring from a reigning scientific model of the brain. Rather, a pluralist hope is a passionate belief that a not-yet unimagined, and therefore indeterminate, future will meliorate current human ills should humans strenuously work toward achieving it. [ABSTRACT FROM AUTHOR]

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This review explores several rarely discussed examples illustrating constructivism principles, generative and selective features of neuronal regulation of behaviour. First, the review highlights Walter Freeman's experiments and mathematical analysis that uncovered the existence of anticipatory attractors, i.e. non-random dynamical patterns in neurodynamics. Since Freeman's work did not extend to neurochemistry, this paper then points to the proposed earlier neurochemical framework summarizing the managerial roles of monoaminergic, cholinergic and opioid receptor systems likely contributing to anticipatory attractors in line with functional constructivism. As a third example, neurochemistry's evidence points to the "Throw & Catch" (T&C) principle in neurodynamics. This principle refers to the pro-active, neurochemically expensive, massive but topical increase of potentials ("Throw") within electrodynamics and neurotransmission in the brain whenever there is an uncertainty in selection of degrees of freedom (DFs). The T&C also underlines the relay-like processes during the selection of DFs. The "Throw" works as an internally generated "flashlight" that, contrarily to the expectations of entropy reduction, increases entropy and variance observed in processes related to orientation and action-formation. The discussed examples highlight the deficiency of structures-oriented projects and excitation-inhibition concepts in neuroscience. The neural regulation of behaviour appears to be a fluid, constructive process, constantly upgrading the choice of behavioural DFs, to ensure the compatibility between the environmental and individual's individuals' needs and capacities. [ABSTRACT FROM AUTHOR]

The Flaviviridae family comprises positive‐sense single‐strand RNA viruses mainly transmitted by arthropods. Many of these pathogens are especially deleterious to the nervous system, and a myriad of neurological symptoms have been associated with infections by Zika virus (ZIKV), West Nile virus (WNV), and Japanese encephalitis virus (JEV) in humans. Studies suggest that viral replication in neural cells and the massive release of pro‐inflammatory mediators lead to morphological alterations of synaptic spine structure and changes in the balance of excitatory/inhibitory neurotransmitters and receptors. Glutamate is the predominant excitatory neurotransmitter in the brain, and studies propose that either enhanced release or impaired uptake of this amino acid contributes to brain damage in several conditions. Here, we review existing evidence suggesting that glutamatergic dysfunction‐induced by flaviviruses is a central mechanism for neurological damage and clinical outcomes of infection. We also discuss current data suggesting that pharmacological approaches that counteract glutamatergic dysfunction show benefits in animal models of such viral diseases. [ABSTRACT FROM AUTHOR]

Chronic low-grade inflammation is associated with a state of diet-induced obesity that impacts systemic tissues and can cross the blood–brain barrier to act directly on the brain. The extent to which pro-inflammatory cytokines released in these conditions affect dopamine presynaptic neurotransmission has not been previously investigated. The purpose of this study was to examine how dopamine terminals are affected by pro-inflammatory cytokines, and to determine if dietary fat consumption potentiates cytokine effects on dopamine release and reuptake rate in the nucleus accumbens (NAc). Male and female C57BL/6J mice were fed high, medium, or low-fat diets (60%, 30%, or 10% total kcals from fat, respectively) for six weeks. Fast scan cyclic voltammetry (FSCV) was used to measure dopamine release and reuptake rate in the NAc core from ex vivo coronal brain slices. Electrically evoked dopamine release and the maximal rate of dopamine reuptake (Vmax) were significantly lower in mice fed the 30% and 60% high-fat diets compared to the 10% low-fat group (p < 0.05). IL-6 5 or 10 nM or TNFα 30 or 300 nM was added to artificial cerebrospinal fluid (aCSF) bathed over brain slices during FSCV. No effect on dopamine release or Vmax was observed with lower concentrations. However, 10 nM IL-6 and 300 nM TNFα significantly reduced dopamine release in the 60% fat group (p < 0.05). No effect of added cytokine was observed on Vmax. Overall, these data provide evidence that dietary fat increases neural responsiveness to cytokines, which may help inform comorbidities between diet-induced obesity and depression or other mood disorders. [ABSTRACT FROM AUTHOR]

IntroductionDimethyl sulfoxide (DMSO) is a widely used solvent to dissolve hydrophobic substances for clinical uses and experimental in vivo purposes. While usually regarded safe, our prior studies suggest changes to behavior following DMSO exposure. We therefore evaluated the effects of a five-day, short-term exposure to DMSO on postnatal infant rats (P6-10).MethodsDMSO was intraperitoneally injected for five days at 0.2, 2.0, and 4.0 ml/kg body mass. One cohort of animals was sacrificed 24 hr after DMSO exposure to analyze the neurometabolic changes in four brain regions (cortex, hippocampus, basal ganglia, and cerebellum) by hydrophilic interaction liquid chromatography. A second cohort of animals was used to analyze chronic alterations to behavior and pathological changes to glia and neuronal cells later in life (P21-P40).Results164 metabolites, including key regulatory molecules (retinoic acid, orotic acid, adrenic acid, and hypotaurine), were found significantly altered by DMSO exposure in at least one of the brain regions at P11 (p

Yukio Yoneda died on 31 December 2023, at 73 years old after a long fight against cancer. He was an eminent neurochemist in academia and industry and also had leadership roles within the International Society for Neurochemistry (ISN) and the Asian Pacific Society for Neurochemistry (APSN) and Japanese Society for Neurochemistry (JSN). Photo credit: Yukio Yoneda provided the APSN with the photo during his service to APSN. [ABSTRACT FROM AUTHOR]

Recent data suggest that 3,4-methylenedioxypyrovalerone (MDPV) has neurotoxic effects; however, the cognitive and neurochemical consequences of MDPV self-administration remain largely unexplored. Furthermore, despite the fact that drug preparations that contain MDPV often also contain caffeine, little is known regarding the toxic effects produced by the co-use of these two stimulants. The current study investigated the degree to which self-administered MDPV or a mixture of MDPV+caffeine can produce deficits in recognition memory and alter neurochemistry relative to prototypical stimulants. Male Sprague Dawley rats were provided 90 min or 12 h access to MDPV, MDPV+caffeine, methamphetamine, cocaine, or saline for 6 weeks. Novel object recognition (NOR) memory was evaluated prior to any drug self-administration history and 3 weeks after the final self-administration session. Rats that had 12 h access to methamphetamine and those that had 90 min or 12 h access to MDPV+caffeine exhibited significant deficits in NOR, whereas no significant deficits were observed in rats that self-administered cocaine or MDPV. Striatal monoamine levels were not systematically affected. These data demonstrate synergism between MDPV and caffeine with regard to producing recognition memory deficits, highlighting the importance of recapitulating the manner in which drugs are used (e.g., in mixtures containing multiple stimulants, binge-like patterns of intake).

Physical activity (PA) promotes brain health in a variety of domains including cognition, mood, and neuroplasticity. At the neurochemical level, the mechanisms underlying these effects in the brain are not fully understood. With proton Magnetic Resonance Spectroscopy (1H-MRS), it is possible to non-invasively quantify metabolite concentrations, enabling studies to obtain measures of exercise-induced neurochemical changes. This systematic review aimed to examine the existing literature on acute effects of PA on brain metabolites as measured by 1H-MRS. Four databases (Cochrane Central Register of Controlled Trials, PubMed, Embase, and PsycINFO) were searched, identifying 2965 studies, of which 9 met the inclusion criteria. Across studies, Gamma-AminoButyric Acid (GABA) and lactate tended to increase after exercise, while no significant changes in choline were reported. For glutamine/glutamate (Glx), studies were inconclusive. Conclusions were limited by the lack of consensus on 1H-MRS data processing and exercise protocols. To reduce inter-study differences, future studies are recommended to: (1) apply a standardized exercise index, (2) consider the onset time of MRS scans, and (3) follow standardized MRS quantification methods.

The basal ganglia are a subcortical collection of interacting clusters of cell bodies, and are involved in reward, emotional, and motor circuits. Within all the brain processing necessary to carry out voluntary movement, the basal nuclei are fundamental, as they modulate the activity of the motor regions of the cortex. Despite being much studied, the motor circuit of the basal ganglia is still difficult to understand for many people at all, especially undergraduate and graduate students. This review article seeks to bring the functioning of this circuit with a simple and objective approach, exploring the functional anatomy, neurochemistry, neuronal pathways, related diseases, and interactions with other brain regions to coordinate voluntary movement. [ABSTRACT FROM AUTHOR]

Brain aging is a naturally occurring process resulting in the decline of cognitive functions and increased vulnerability to develop age‐associated disorders. Fluctuation in lipid species is crucial for normal brain development and function. However, impaired lipid metabolism and changes in lipid composition in the brain have been increasingly recognized to play a crucial role in physiological aging, as well as in several neurodegenerative diseases. In the last decades, the role of sexual dimorphism in the vulnerability to develop age‐related neurodegeneration has increased. However, further studies are warranted for detailed assessment of how age, sex, and additional non‐biological factors may influence the lipid changes in brains. The aim of this work is to address the presence of sex differences in the brain lipid changes that occur along aging, and in the two most common age‐related neurodegenerative disorders (Alzheimer's and Parkinson's diseases). We included the studies that assessed lipid‐related alterations in the brain of both humans and experimental models. Additionally, we explored the influence of sex on lipid‐lowering therapies. We conclude that sex exerts a notable effect on lipid modifications occurring with age and neurodegeneration, and in lipid‐reducing interventions. Therefore, the application of sex as an experimental variable is strongly encouraged for future research in the field of precision medicine approach. [ABSTRACT FROM AUTHOR]