J. Neurosci. Res. [JOURNAL]
Sun
200 papers
MRI-T2 Relaxometry is Increased in Mild Traumatic Brain Injury: Indications of Acute Brain Abnormalities After Injury.
Bedggood MJ, Essex CA, Theadom A … +5 more , Murray H, Hume P, Holdsworth SJ, Faull RLM, Pedersen M
J Neurosci Res · 2025 Apr · PMID 40178334 · Full text
Mild traumatic brain injury (mTBI) is a common condition, particularly pervasive in contact sports environments. A range of symptoms can accompany this type of injury and negatively impact people's lives. As mTBI diagnos...
Mild traumatic brain injury (mTBI) is a common condition, particularly pervasive in contact sports environments. A range of symptoms can accompany this type of injury and negatively impact people's lives. As mTBI diagnosis and recovery largely rely on subjective reports, more objective injury markers are needed. The current study compared structural brain MRI-T2 relaxometry between a group of 40 male athletes with mTBI within 14 days of injury and 40 age-matched male controls. Voxel-averaged T2 relaxometry within the gray matter was increased for the mTBI group compared to controls (p < 0.001), with statistically significant increased T2 relaxometry particularly in superior cortical regions. Our findings indicate subtle brain abnormalities can be identified in acute mTBI using MRI-T2 relaxometry. These brain abnormalities may reflect inflammation present in the brain and could constitute an objective injury marker to supplement current subjective methods that dominate clinical decisions regarding diagnosis and prognosis. Future research should validate this potential marker with other data types, such as blood biomarkers or histological samples.
Synaptic Function and Dysfunction: New Frontiers in CNS Disorders.
Aslan FS, Akdag MB, Doganyigit Z … +3 more , Okan A, Shaikh MF, Akyuz E
J Neurosci Res · 2025 Apr · PMID 40172089 · Publisher ↗
Central nervous system (CNS) disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and migraines, rank among the most prevalent and concerning conditions worldwide. Despite ongoi...
Central nervous system (CNS) disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and migraines, rank among the most prevalent and concerning conditions worldwide. Despite ongoing research, the pathophysiology of these disorders remains incompletely understood, primarily due to their complex etiology. Current pharmacological treatments mainly focus on alleviating symptoms rather than addressing the underlying causes of these diseases. CNS disorders are marked by impairments in neurocognitive and neuromuscular functions, and cognitive processes like learning and memory. This deterioration not only impacts the quality of life of affected individuals but also places a significant burden on their families. Neuroplasticity is a key property of the nervous system that enables brain repair and functional recovery. However, in CNS disorders, neuroplasticity is often compromised. Neuroplasticity, which is regulated by gene expression, is also modulated by environmental factors and epigenetic mechanisms, thereby reshaping neuronal networks in response to various biological and environmental stimuli and brain function. Importantly, neuroplasticity plays a critical role in repairing the brain, especially in the context of neurodegenerative diseases, where damaged neurons can reorganize and re-establish lost functions. Targeting neuroplasticity mechanisms holds significant potential for developing therapeutic interventions to improve treatment outcomes and prevent CNS disorders. A deeper understanding of neuroplasticity in neurological diseases could open new avenues for enhancing patient quality of life. This review aims to provide a comprehensive overview of synaptic function and the neuroplasticity mechanisms that are disrupted in neurological disorders.
An Interplay Between Hypothalamic Microstructure, Systemic Metabolism and Gut Microbiome Composition in Male Rats at Hyperacute Timepoint Post TBI.
Arora P, Kumari M, Singh K … +4 more , Devi MM, Rana P, Sandhir R, Trivedi R
J Neurosci Res · 2025 Apr · PMID 40167488 · Publisher ↗
Traumatic brain injury (TBI) is an insult to the brain that impacts neuronal and non-neuronal cells/tissues. The study aimed to understand TBI-induced early changes in the brain and systemic physiology. The male rats wer...
Traumatic brain injury (TBI) is an insult to the brain that impacts neuronal and non-neuronal cells/tissues. The study aimed to understand TBI-induced early changes in the brain and systemic physiology. The male rats were subjected to mild and moderate TBI, where serum and urine metabolic fingerprints of mild TBI rats showed a hypermetabolic response with increased energy metabolites, amino acids, and gut metabolites in serum and increased TCA cycle intermediates in urine. In contrast, the moderate TBI rats showed decreased lactate, pyruvate, amino acids (glycine and leucine) and gut metabolites [trimethylamine N OXIDE (TMAO), choline and acetate] in serum. The urine showed increased pyruvate, creatinine, and allantoin levels. To understand the brain's role in altered metabolic physiology, hypothalamus structure was assessed using diffusion tensor imaging (DTI) and stress levels were observed using serum corticosterone. The injured rats exhibited changes in DTI metrics in the hypothalamus, suggesting a potential disruption in the regulation of the hypothalamus-pituitary-adrenal axis (HPA) axis. These alterations were accompanied by increased TNF-α levels after moderate TBI. The injury induced allostatic overload, accompanied by impaired hypothalamic structure, and metabolic physiology also showed gut microbiome dysbiosis. The gut microbiome showed an increased Firmicutes: Bacteroidetes ratio after injury, with variable gut composition after both injuries. Therefore, the present study provides insight into an interplay between the HPA axis, metabolism, and gut microbiome following TBI. Importantly, this crosstalk between the regulatory systems was different after mild and moderate injury, highlighting the need to assess injury phenotype based on the severity.
Dynamic Temporal Alterations of the Cerebellum in Parkinson's Disease With Different Dominant-Affected Sides.
Chen L, Wang J, Gao L … +3 more , Sun J, Zhang D, Wu T
J Neurosci Res · 2025 Mar · PMID 40041986 · Publisher ↗
Laterality of motor deficits is a hallmark of Parkinson's disease (PD), which is strongly correlated with disease progression. The cerebellum is an important node in the motor-related network in PD. However, the role of...
Laterality of motor deficits is a hallmark of Parkinson's disease (PD), which is strongly correlated with disease progression. The cerebellum is an important node in the motor-related network in PD. However, the role of the cerebellum in PD lateralization remains unclear. This study enrolled 48 left-dominant-affected PD patients (LPD), 60 right-dominant-affected PD patients (RPD) and 92 age- and sex-matched healthy controls (HCs). We utilized dynamic functional connectivity and co-activation pattern analysis to investigate dynamic alterations of the cerebellum between PD patients and HCs by resting-state fMRI. Pearson partial correlation was used to measure brain-clinical correlations. We revealed two states and five co-activation patterns during the scans. Compared to HCs and RPD, LPD patients more frequently displayed State II and persisted in this state for a more extended period. The mean dwell time (MDT) in State II rose from HCs to RPD and to LPD. The MDT in State II was positively correlated with sleep disturbance in LPD patients. Regarding co-activation patterns (CAPs), LPD and RPD patients were less likely to exhibit CAP2. LPD patients were less likely to demonstrate CAP1 compared to HCs. The CAP1 metrics were positively associated with motor deficits in LPD patients. These results revealed the dynamic alterations of the cerebellum in different dominant-affected PD patients, which were related to motor deficits and sleep disturbances in PD patients. Our findings suggest that the dynamic cerebellar features may be significant factors in the lateralization of PD.
Magnetic Resonance Imaging and Anatomical Correlation of Human Temporal Lobe Landmarks in 3D Euclidean Space: A Study of Control and Epilepsy Disease Subjects.
Delgado-González JC, Delgado-Gandía C, Delgado-Gandía C … +3 more , Cebada-Sánchez S, De-La-Rosa-Prieto C, Artacho-Pérula E
J Neurosci Res · 2025 Feb · PMID 39989215 · Publisher ↗
Epilepsy is a common neurological disorder of great importance to patients and society. Sclerosis is associated with neuronal loss and neurodegeneration in specific regions of the hippocampal formation. The hippocampal f...
Epilepsy is a common neurological disorder of great importance to patients and society. Sclerosis is associated with neuronal loss and neurodegeneration in specific regions of the hippocampal formation. The hippocampal formation and temporal lobe are not the only regions affected; the chronicity of the disease extends the involvement to other brain regions. Our aim is to investigate the spatial relationship of anatomical structures in both control (CO) and epileptic (EP) subjects using magnetic resonance imaging (MRI) in order to determine changes in epileptic patients compared to healthy anatomical structures. Anatomical landmarks are identified and registered in 3D space to provide a reference for the brain structures; the 3D network is described quantitatively using planar distances, as well as measuring rostrocaudal and Euclidean distances. The planar and rostrocaudal distances are the most remarkable discriminators between CO and EP groups, especially between structures located in and outside the temporal lobe. The study achieves a 100% discrimination between the control group and the epileptic group with the discriminant use of two distances: D_PL, Hpe/Cde and D_RC, As/cae. Finally, discriminates 100% between the three study groups, control group CO, extratemporal lobe epilepsy ETLE and temporal lobe epilepsy TLE, with a total of 12 distances distributed in the three axes of space. This study allows us to hope for a future application, its clinical utility may allow us not only to identify processes (in our case, epilepsy), but also to obtain parameters of the evolution of the disease.
Human Induced Pluripotent Stem Cells: Directed Differentiation Methods and Applications in Brain Diseases.
Wang Y, Wang Z, Wang L … +6 more , Sun Y, Song H, Cheng X, He X, Gao Z, Sun Y
J Neurosci Res · 2025 Feb · PMID 39935271 · Publisher ↗
Human induced pluripotent stem cells (hiPSCs), similar to embryonic stem cells, are a class of pluripotent stem cells with the potential to differentiate into various kinds of cells. Because the application of hiPSCs obt...
Human induced pluripotent stem cells (hiPSCs), similar to embryonic stem cells, are a class of pluripotent stem cells with the potential to differentiate into various kinds of cells. Because the application of hiPSCs obtained by reprogramming patients' somatic cells in the treatment of brain diseases bypasses the ethical constraints on the use of embryonic stem cells and mitigates immune rejection, hiPSCs have profound clinical application prospects. In this review, we first summarized the differentiation methods of hiPSCs into different kinds of neurons, and secondly discussed the application of hiPSCs in several brain disease models, so as to provide a reference for the future application of hiPSCs in the studies and treatment of brain diseases.
Transcorneal Electrical Stimulation Modulates Visual Pathway Function in Mice.
Castoldi V, Rossi E, Marenna S … +2 more , Comi G, Leocani L
J Neurosci Res · 2025 Feb · PMID 39931921 · Full text
Due to its ability to modulate neuronal activity, electrical stimulation of the eye may be a promising therapy for preserving or restoring vision. To investigate how electrical currents can influence visual function, Tra...
Due to its ability to modulate neuronal activity, electrical stimulation of the eye may be a promising therapy for preserving or restoring vision. To investigate how electrical currents can influence visual function, Transcorneal Electrical Stimulation (TES) was tested on both female and male C57BL/6 mice to evaluate its neuromodulatory effect from the retina to the cerebral cortex through visual evoked potential (VEP) and electroretinogram (ERG) recording. VEP or ERG was acquired before (baseline), immediately (t0), after 5 min (t5), and 10 min (t10) of sham (i.e., no stimulation) or TES applied on the eye of anesthetized C57BL/6 mice. Notably, TES affected neuronal activity in the visual pathway since a significant increase in VEP and ERG amplitude was detected and persisted 10 min after TES. The amplitude increase induced by TES could underlie an enhancement of neuronal excitability that may ameliorate retinal-genicular-cortical function in diseases involving the visual system.
EXPRESSION OF CONCERN: Role of the Nrf2-ARE Pathway in Early Brain Injury After Experimental Subarachnoid Hemorrhage.
J Neurosci Res · 2025 Feb · PMID 39930956 · Publisher ↗
Abstract loading — click title to view on PubMed.
Klf10 Regulates the Emergence of Glial Phenotypes During Hypothalamic Development.
Garduño-Tamayo NA, Almazán JL, Romo-Rodríguez R … +6 more , Valle-García D, Meza-Sosa KF, Pérez-Domínguez M, Pelayo R, Pedraza-Alva G, Pérez-Martínez L
J Neurosci Res · 2025 Feb · PMID 39924964 · Full text
Glial cells play a pivotal role in the Central Nervous System (CNS), constituting most brain cells. Gliogenesis, crucial in CNS development, occurs after neurogenesis. In the hypothalamus, glial progenitors first generat...
Glial cells play a pivotal role in the Central Nervous System (CNS), constituting most brain cells. Gliogenesis, crucial in CNS development, occurs after neurogenesis. In the hypothalamus, glial progenitors first generate oligodendrocytes and later astrocytes. However, the precise molecular mechanisms governing the emergence of glial lineages in the developing hypothalamus remain incompletely understood. This study reveals the pivotal role of the transcription factor KLF10 in regulating the emergence of both astrocyte and oligodendrocyte lineages during embryonic hypothalamic development. Through transcriptomic and bioinformatic analyses, we identified novel KLF10 putative target genes, which play important roles in the differentiation of neurons, astrocytes, and oligodendrocytes. Notably, in the absence of KLF10, there is an increase in the oligodendrocyte population, while the astrocyte population decreases in the embryonic hypothalamus. Strikingly, this decline in the number of astrocytes persists into adulthood, indicating that the absence of KLF10 leads to an extended period of oligodendrocyte emergence while delaying the appearance of astrocytes. Our findings also unveil a novel signaling pathway for Klf10 gene expression regulation. We demonstrate that Klf10 is a target of CREB and that its expression is upregulated via the BDNF-p38-CREB pathway. Thus, we postulate that KLF10 is an integral part of the hypothalamic developmental program that ensures the correct timing for glial phenotypes' generation. Importantly, we propose that the Klf10 mouse model represents a valuable tool for investigating the impact of reduced astrocyte and microglia populations in the homeostasis of the adult hypothalamus.
The Utility of Prolonged Chronic Unpredictable Stress to Study the Effects of Chronic Fluoxetine, Eicosapentaenoic Acid, and Lipopolysaccharide on Anxiety-Like Behavior and Hippocampal Transcriptomic Responses in Male Rats.
Demin KA, Kolesnikova TO, Galstyan DS … +9 more , Krotova NA, Ilyin NP, Derzhavina KA, Seredinskaya M, Nerush M, Pushkareva SA, Masharsky A, de Abreu MS, Kalueff AV
J Neurosci Res · 2025 Feb · PMID 39907099 · Publisher ↗
Chronic stress is a common trigger of multiple neuropsychiatric illnesses. Animal models are widely used to study stress-induced brain disorders and their interplay with neuroinflammation and other neuroimmune processes....
Chronic stress is a common trigger of multiple neuropsychiatric illnesses. Animal models are widely used to study stress-induced brain disorders and their interplay with neuroinflammation and other neuroimmune processes. Here, we apply the prolonged 12-week chronic unpredictable stress (PCUS) model to examine rat behavioral and hippocampal transcriptomic responses to stress and to chronic 4-week treatment with a classical antidepressant fluoxetine, an anti-inflammatory agent eicosapentaenoic acid (EPA), a pro-inflammatory agent lipopolysaccharide and their combinations. Overall, PCUS evoked anxiety-like behavioral phenotype in rats, corrected by chronic fluoxetine (alone or combined with other drugs), and EPA. PCUS also evoked pronounced transcriptomic responses in rat hippocampi, involving > 200 differentially expressed genes. While pharmacological manipulations did not affect hippocampal gene expression markedly, Gpr6, Drd2 and Adora2a were downregulated in stressed rats treated with fluoxetine, EPA and fluoxetine + EPA, suggesting their respective protein products (G protein-coupled receptor 6, dopamine D2 receptor and adenosine A2A receptor) as potential evolutionarily conserved targets under chronic stress. Overall, these findings support the validity of rat PCUS paradigm as a useful model to study stress-related anxiety pathogenesis, and call for further research probing how various conventional and novel drugs may (co)modulate behavioral and neurotranscriptomic biomarkers of chronic stress.
Acute Intermittent Theta-Burst Stimulation Produces Antidepressant-Like Effects by Modulating Neuronal Oscillations and Serotonin Levels of the Medial Prefrontal Cortex in Experimental Parkinson's Disease.
Wang Y, Liu J, Hui Y … +8 more , Wu Z, Wu X, Bai Y, Li J, Zhang L, Liu K, Zhang Q, Li L
J Neurosci Res · 2025 Feb · PMID 39902890 · Publisher ↗
Parkinson's disease (PD)-related depression is associated with aberrant neuronal oscillations and 5-hydroxytryptamine (5-HT) neurotransmission in the medial prefrontal cortex (mPFC). Intermittent theta-burst stimulation...
Parkinson's disease (PD)-related depression is associated with aberrant neuronal oscillations and 5-hydroxytryptamine (5-HT) neurotransmission in the medial prefrontal cortex (mPFC). Intermittent theta-burst stimulation (iTBS), an updated pattern of high-frequency repetitive transcranial magnetic stimulation, has possible efficacy in PD-related depression. However, whether iTBS alleviates PD-related depression through modulating neuronal oscillations and 5-HT levels in the mPFC has not been determined. In this study, male Sprague-Dawley rats were used to establish a unilateral 6-hydroxydopamine-induced PD model. Then, acute iTBS was applied to the parkinsonian rats, and behavioral, neurochemical, and electrophysiological experiments were performed. We found that the parkinsonian rats exhibited increased immobility time and decreased sucrose preference accompanied by an increase of δ power and a decrease of θ power in the mPFC compared to sham-operated rats. One block of iTBS (1 block-iTBS, 300 stimuli) alleviated depressive-like behaviors in parkinsonian rats and elevated 5-HT levels in the mPFC compared to sham-iTBS. Additionally, it altered neuronal oscillations in the mPFC in the opposite fashion by suppressing the δ rhythm and enhancing the θ and β rhythms compared to sham-iTBS, suggesting that acute iTBS induces hyperactivity in the mPFC. With this iTBS paradigm, we also observed decreased parvalbumin expression in the mPFC, reflecting reduced cortical inhibition. Finally, correlation analyses showed strong correlation between immobility time and θ power after 1 block-iTBS. These findings suggest that the application of acute iTBS in parkinsonian rats produces antidepressant-like effects, which may be associated with elevated 5-HT levels and normalized neuronal oscillations in the mPFC.
Tale of Two n-Backs: Diverging Associations of Dorsolateral Prefrontal Cortex Activation With n-Back Task Performance.
Tubiolo PN, Williams JC, Van Snellenberg JX
J Neurosci Res · 2025 Feb · PMID 39902779 · Full text
In studying the neural correlates of working memory (WM) ability via functional magnetic resonance imaging (fMRI) in health and disease, it is relatively uncommon for investigators to report associations between brain ac...
In studying the neural correlates of working memory (WM) ability via functional magnetic resonance imaging (fMRI) in health and disease, it is relatively uncommon for investigators to report associations between brain activation and measures of task performance. Additionally, how the choice of WM task impacts observed activation-performance relationships is poorly understood. We sought to illustrate the impact of WM task on brain-behavior correlations using two large, publicly available datasets. We conducted between-participants analyses of task-based fMRI data from two publicly available datasets: The Human Connectome Project (HCP; n = 866) and the Queensland Twin Imaging (QTIM) Study (n = 459). Participants performed two distinct variations of the n-back WM task with different stimuli, timings, and response paradigms. Associations between brain activation ([2-back - 0-back] contrast) and task performance (2-back % correct) were investigated separately in each dataset, as well as across datasets, within the dorsolateral prefrontal cortex (dlPFC), medial prefrontal cortex, and whole cortex. Global patterns of activation to task were similar in both datasets. However, opposite associations between activation and task performance were observed in bilateral pre-supplementary motor area and left middle frontal gyrus. Within the dlPFC, HCP participants exhibited a significantly greater activation-performance relationship in bilateral middle frontal gyrus relative to QTIM Study participants. The observation of diverging activation-performance relationships between two large datasets performing variations of the n-back task serves as a critical reminder for investigators to exercise caution when selecting WM tasks and interpreting neural activation in response to a WM task.
Associations Between the Neural Stress Response and Symptoms of Anxiety and Depression.
Giglberger M, Peter HL, Henze GI … +6 more , Bärtl C, Konzok J, Kirsch P, Kudielka BM, Kreuzpointner L, Wüst S
J Neurosci Res · 2025 Jan · PMID 39817876 · Full text
Anxiety and depression disorders show high prevalence rates, and stress is a significant risk factor for both. However, studies investigating the interplay between anxiety, depression, and stress regulation in the brain...
Anxiety and depression disorders show high prevalence rates, and stress is a significant risk factor for both. However, studies investigating the interplay between anxiety, depression, and stress regulation in the brain are scarce. The present manuscript included 124 law students from the LawSTRESS project. Anxiety and depression symptoms were assessed using the Hospital Anxiety and Depression Scale (HADS), and psychosocial stress was induced with the imaging stress paradigm ScanSTRESS. Anxiety, but not depression scores, were significantly related to neural stress responses in a striato-limbic cluster. Moreover, relative to women, men showed stronger associations between anxiety scores and activation in striatal and temporal clusters. A bifactor model of the HADS suggested a general factor characterized by tension, nervousness, and cheerlessness, which was associated with activation changes in a similar but more circumscribed cluster than anxiety. In the LawSTRESS project, the HADS was assessed at five sampling points (1 year, 3 months, 1 week prior exam, 1 week, and 1 month thereafter), and thus an exploratory trajectory analysis could be performed. It confirmed the relationship between anxiety scores and striatal stress responses at baseline but revealed no predictive value of the neural measure across the sampling points. Our results suggest that-in healthy young participants-neural acute psychosocial stress responses in striato-limbic structures are associated with anxiety, supporting the assumption that these regions are related to individual differences in vulnerability to stress-related disorders. A correlation with depression scores could not be found, and possible explanations are discussed.
Neurological and Cognitive Effects of Hypothyroidism in Patients With Epilepsy: A Study on Anti-Seizure Medicines Therapy.
Molodozhnikova N, Prokhorova S, Monov D … +1 more , Lilyanov N
J Neurosci Res · 2025 Jan · PMID 39797431 · Publisher ↗
The primary objective of this study was to examine neurological disorders and cognitive impairments in patients with secondary hypothyroidism and epilepsy undergoing treatment with antiepileptic medications. The study in...
The primary objective of this study was to examine neurological disorders and cognitive impairments in patients with secondary hypothyroidism and epilepsy undergoing treatment with antiepileptic medications. The study included 184 patients divided into three groups: Group 1 (subclinical hypothyroidism, n = 60), Group 2 (manifest hypothyroidism, n = 64), and Group 3 (control, n = 60). Patients in Group 2 received levothyroxine therapy (initial dose of 25 μg/day, titrated to 50-100 μg/day), while Groups 1 and 2 were treated with anti-seizure medications (valproic acid, 40 mg/kg/day). Neurological symptoms, including Babinski's reflex abnormalities (χ = 8.15, p = 0.017) and sensory disturbances (χ = 12.44, p = 0.005), were significantly more frequent in Group 2 than in Group 1. Cognitive test scores were significantly lower in Group 2 compared to Group 3 across all domains (F(2, 181) = 6.55, p = 0.002 for MMSE; F(2, 181) = 4.70, p = 0.010 for FAB; and F(2, 181) = 5.75, p = 0.006 for CDT), with Group 1 showing intermediate results. Regression analysis identified neurodegenerative disease risk (β = 0.34, CI: 0.20-0.48, p < 0.001), anemia (β = 0.32, CI: 0.15-0.49, p = 0.001), and prolonged stress (β = 0.26, CI: 0.12-0.40, p = 0.002) as significant predictors of cognitive decline, while higher education was protective (β = -0.28, CI: -0.42 to -0.14, p = 0.003). An inverse relationship was observed between TSH levels and cognitive scores (r = -0.55, p < 0.001).
Mechanisms of Autophagy in Ineffective Reperfusion After Ischemic Stroke.
Bai S, Ding Y, Simo L … +2 more , Li F, Geng X
J Neurosci Res · 2025 Jan · PMID 39764666 · Publisher ↗
Despite significant advancements in achieving high recanalization rates (80%-90%) for large vessel occlusions through mechanical thrombectomy, the issue of "futile recanalization" remains a major clinical challenge. Futi...
Despite significant advancements in achieving high recanalization rates (80%-90%) for large vessel occlusions through mechanical thrombectomy, the issue of "futile recanalization" remains a major clinical challenge. Futile recanalization occurs when over half of patients fail to experience expected symptom improvement after vessel recanalization, often resulting in severe functional impairment or death. Traditionally, this phenomenon has been attributed to inadequate blood flow and reperfusion injury. More recently, ongoing neuronal death after reperfusion, which leads to the progression of the ischemic penumbra into the core infarct, has been termed "futile reperfusion." This review explores the complex role of autophagy mechanisms in futile reperfusion following ischemic stroke, with a focus on its relationship to neuronal survival. We also examine the regulation of autophagic activity by epigenetic mechanisms. By investigating autophagy's role in ischemic stroke, we aim to identify novel pathways for precision treatment.
The Intricate Interplay: Microbial Metabolites and the Gut-Liver-Brain Axis in Parkinson's Disease.
Kollaparampil Kishanchand D, K A AK, Chandrababu K … +3 more , Philips CA, Sivan U, Pulikaparambil Sasidharan BC
J Neurosci Res · 2025 Jan · PMID 39754366 · Publisher ↗
Parkinson's Disease (PD) is a neurodegenerative disorder marked by the depletion of dopaminergic neurons. Recent studies highlight the gut-liver-brain (GLB) axis and its role in PD pathogenesis. The GLB axis forms a dyna...
Parkinson's Disease (PD) is a neurodegenerative disorder marked by the depletion of dopaminergic neurons. Recent studies highlight the gut-liver-brain (GLB) axis and its role in PD pathogenesis. The GLB axis forms a dynamic network facilitating bidirectional communication between the gastrointestinal tract, liver, and central nervous system. Dysregulation within this axis, encompassing gut dysbiosis and microbial metabolites, is emerging as a critical factor influencing PD progression. Our understanding of PD was traditionally centered on neurodegenerative processes within the brain. However, examining PD through the lens of the GLB axis provides new insights. This review provides a comprehensive analysis of microbial metabolites, such as short-chain fatty acids (SCFAs), trimethylamine-N-oxide (TMAO), kynurenine, serotonin, bile acids, indoles, and dopamine, which are integral to PD pathogenesis by modulation of the GLB axis. Our extensive research included a comprehensive literature review and database searches utilizing resources such as gutMGene and gutMDisorder. These databases have been instrumental in identifying specific microbes and their metabolites, shedding light on the intricate relationship between the GLB axis and PD. This review consolidates existing knowledge and underscores the potential for targeted therapeutic interventions based on the GLB axis and its components, which offer new avenues for future PD research and treatment strategies. While the GLB axis is not a novel concept, this review is the first to focus specifically on its role in PD, highlighting the importance of integrating the liver and microbial metabolites as central players in the PD puzzle.
Correction to Sensory Perception of Environmental Cues as a Modulator of Aging and Neurodegeneration: Insights From Caenorhabditis elegans.
J Neurosci Res · 2025 Jan · PMID 39745007 · Publisher ↗
Abstract loading — click title to view on PubMed.
RETRACTION: Nuclear Receptor nur77 Promotes Cerebral Cell Apoptosis and Induces Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats.
J Neurosci Res · 2025 Jan · PMID 39743835 · Publisher ↗
Y. Dai, W. Zhang, Q. Sun, X. Zhang, X. Zhou, Y. Hu, and J. Shi, "Nuclear Receptor nur77 Promotes Cerebral Cell Apoptosis and Induces Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats," Journal of Neur...
Y. Dai, W. Zhang, Q. Sun, X. Zhang, X. Zhou, Y. Hu, and J. Shi, "Nuclear Receptor nur77 Promotes Cerebral Cell Apoptosis and Induces Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats," Journal of Neuroscience Research 92, no. 9 (2014): 1110-1121. https://doi.org/10.1002/jnr.23392. The above article, published online on April 15, 2014 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editors-in-Chief, Cristina A. Ghiani and J. Paula Warrington, and Wiley Periodicals LLC. The journal received a report from a third party, which described image overlap between the B1 and C1 panels and the A4 and B4 panels in Figure 6. In addition, a third party also indicated that the majority of images in Figure 5 had been used in another article by many of the same authors (Dai et al. 2014 [https://doi.org/10.1016/j.brainres.2014.01.052]) and that images in Figure 4 had been re-used in a separate article also by many of the same authors (Dai et al. 2014 [https://doi.org/10.1007/s11064-014-1355-6]). The authors did not respond to multiple requests from the publisher for the original data and an explanation. The retraction has been agreed to because of the evidence of image duplications both within this article and between other articles by many of the same authors, which fundamentally compromises the conclusions presented in this article. The authors did not respond to our notice regarding the Retraction.
Hippocampal Lesions in Male Rats Produce Retrograde Memory Loss for Over-Trained Spatial Memory but Do Not Impact Appetitive-Contextual Memory: Implications for Theories of Memory Organization in the Mammalian Brain.
Hong NS, Lee JQ, Bonifacio CJT … +9 more , Gibb MJ, Kent M, Nixon A, Panjwani M, Robinson D, Rusnak V, Trudel T, Vos J, McDonald RJ
J Neurosci Res · 2025 Jan · PMID 39743833 · Full text
Evidence suggests that hippocampal (HPC) disruption following learning produces retrograde amnesia on a range of tasks. Many of these tasks do not require HPC function in the anterograde direction suggesting that, in the...
Evidence suggests that hippocampal (HPC) disruption following learning produces retrograde amnesia on a range of tasks. Many of these tasks do not require HPC function in the anterograde direction suggesting that, in the intact brain, the HPC is actively involved during all forms of learning. However, prior work has also demonstrated double dissociations of HPC and amygdala function, which is inconsistent with this view. Here, we aim to understand this discrepancy by assessing the effects of neurotoxic lesions of the HPC on anterograde and retrograde amnesia for conditioned place preference (CPP). This task is dependent on a network centered on the basolateral amygdala and not the HPC. The results show that extensive HPC damage had no impact on the acquisition or expression of CPP. One explanation for this result is that the task requires multiple, distributed training sessions for conditioning to emerge, and it has been proposed that this parameter may eliminate the need for HPC to support memory. To test this, we completed experiments to probe place learning in the Morris water task, which is thought to always require HPC function, but implemented an over-training procedure before HPC damage. We found that rats were severely impaired suggesting that this task parameter does not always allow non-HPC networks to support learning. Finally, an experiment was designed to test whether memories acquired by distinct memory networks on the same days, within hours of one another, would be linked in HPC. The results showed that they remained independent of one another.
Insights Into Retinal Pathologies in Neurological Disorders: A Focus on Parkinson's Disease, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Alzheimer's Disease.
Akyuz E, Aslan FS, Hekimoglu A … +1 more , Yilmaz BN
J Neurosci Res · 2025 Jan · PMID 39737769 · Publisher ↗
Neurological diseases are central nervous system (CNS) disorders affecting the whole body. Early diagnosis of the diseases is difficult due to the lack of disease-specific tests. Adding new biomarkers external to the CNS...
Neurological diseases are central nervous system (CNS) disorders affecting the whole body. Early diagnosis of the diseases is difficult due to the lack of disease-specific tests. Adding new biomarkers external to the CNS facilitates the diagnosis of neurological diseases. In this respect, the retina has a common embryologic origin with the CNS. Retinal imaging technologies including optical coherence tomography (OCT) can be used in the understanding and processual monitoring of neurological diseases. Retinal imaging has been recently recognized as a potential source of biomarkers for neurological diseases, increasing the number of studies in this direction. In this review, the association of retinal abnormalities with Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD) is explained. Structural and functional abnormalities in retina as a predictive marker may facilitate early diagnosis of diseases. Although not all retinal abnormalities are predictive of neurologic diseases, changes in the retinal layers including retinal pigment epithelium and plexiform layers should suggest the risk of PD, MS, ALS, and AD.
About
- Frequency
- Sun
- Papers found
- 200
- RSS feed
- Subscribe