A5072809551- Parkinson's Disease Mechanisms and Treatments
- Alzheimer's disease research and treatments
- Neural dynamics and brain function
- Photoreceptor and optogenetics research
- Neuroendocrine regulation and behavior
- Neuroscience and Neuropharmacology Research
- Peptidase Inhibition and Analysis
- Nuclear Receptors and Signaling
- Cellular transport and secretion
- Protease and Inhibitor Mechanisms
- Neurological diseases and metabolism
- Autism Spectrum Disorder Research
- Macrophage Migration Inhibitory Factor
- Neurological disorders and treatments
- Biochemical and Structural Characterization
- Air Quality and Health Impacts
- Receptor Mechanisms and Signaling
- Ginkgo biloba and Cashew Applications
- Nerve injury and regeneration
- Circadian rhythm and melatonin
- Neurobiology and Insect Physiology Research
- Neuropeptides and Animal Physiology
- Prion Diseases and Protein Misfolding
- Barrier Structure and Function Studies
- S100 Proteins and Annexins
Wuhan University
2021-2024
Renmin Hospital of Wuhan University
2021-2024
Zhejiang Lab
2020-2024
Zhejiang University
2020-2024
Second Affiliated Hospital of Zhejiang University
2020-2021
Abstract The aggregation and prion-like propagation of α-synuclein are involved in the pathogenesis Parkinson’s disease. However, underlying mechanisms regulating assembly spreading fibrils remain poorly understood. Tau co-deposits with brains disease patients, suggesting a pathological interplay between them. Here we show that tau interacts accelerates its aggregation. Compared pure fibrils, tau-modified enhanced seeding activity, inducing mitochondrial dysfunction, synaptic impairment...
ABSTRACT Background The deposition of α‐synuclein (α‐Syn) in the brain is pathological hallmark Parkinson's disease (PD). Epidemiological data indicate that exposure to fine particulate matter (≤2.5 μm aerodynamic diameter [PM2.5]) associated with an increased risk for PD. Objective aim this study investigate whether PM2.5 has a direct effect on α‐Syn pathology and how it drives Methods was added into monomers different cell models test can promote fibrillization aggregation α‐Syn. A53T...
Although aggressive behaviors are universal and essential for survival, "uncontrollable" abnormal in animals or humans may have severe adverse consequences social costs. Neural circuits regulating specific forms of aggression under defined conditions been described, but how brain govern a general response remains unknown. Here, we found that posterior substantia innominata (pSI) neurons responded to several aggression-provoking cues with the graded activity differential dynamics, predicting...
Parkinson's disease (PD) is characterized by the pathologic aggregation and prion-like propagation of α-synuclein (α-syn). Emerging evidence shows that fungal infections increase incidence PD. However, molecular mechanisms which fungi promote onset PD are poorly understood. Here, we show nasal infection with Saccharomyces cerevisiae (S. cerevisiae) in α-syn A53T transgenic mice accelerates α-syn. Furthermore, found Sup35, a prion protein from S. cerevisiae, key factor initiating pathology...
Parkinson's disease (PD) is one of the most common neurodegenerative diseases, which characterized by loss dopaminergic neurons in nigrostriatal pathway. Synaptic dysfunction impairs dopamine turnover and contributes to degeneration neurons. However, molecular mechanisms underlying synaptic neuronal vulnerability PD are not clear. Here, we report that synaptojanin 1 (SYNJ1), a polyphosphoinositide phosphatase concentrated at nerve terminals, substrate cysteine proteinase, asparagine...
Parkinson's disease (PD) is the most common motor-associated neurodegenerative disease. Although pathogenesis of PD still wrapped in mist, accumulating evidence indicates that mitochondrial dysfunction contributes to onset and progression PD. We previously reported lysosomal protease asparagine endopeptidase (AEP) cleaves α-synuclein brains patients. The major product, 1–103, significantly promotes PD-like histological changes motor dysfunction. However, underlying molecular mechanisms...
Neurofibrillary tangles composed of hyperphosphorylated tau and synaptic dysfunction are characteristics Alzheimer’s disease (AD). However, the underlying molecular mechanisms remain poorly understood. Here, we identified Amphiphysin I mediates both phosphorylation in AD. is cleaved by a cysteine proteinase asparagine endopeptidase (AEP) at N278 brains AD patients. The amount AEP-generated N-terminal fragment (1-278) increased with aging. inhibits clathrin-mediated endocytosis induces...
The accumulation of amyloid-β (Aβ) and overactivation microglia contribute to the pathogenesis Alzheimer's disease (AD), but interaction between microglial activation Aβ deposition in AD remains elusive. Here we revealed that activates promotes release Galectin-9 (Gal-9), a member β-galactoside-binding family lectins. levels Gal-9 cerebrospinal fluid brain tissues patients are higher than those control subjects. interacts with its aggregation, generating Gal-9-Aβ fibrils enhanced seeding...
Parkinson's disease (PD) is one of the most common neurodegenerative disorders. However, its cellular and molecular mechanisms still wrap in mist. This partially caused by absence appropriate animal models mimicking sporadic PD that constitutes majority cases. Previously, we reported a cysteine protease, asparagine endopeptidase (AEP), activated an age-dependent manner, cleaves α-synuclein brain patients. The AEP-derived 1-103 fragment required for pathogenesis PD. Thus, designed...
Abstract Aggression behaviors typically vary between sexes, but the molecular mechanisms driving these disparities in neural coding are unclear. We found that aggression selectively activates GABAergic neurons posterior substantia innominata (pSI), an extend amygdala region critical for aggressive both sexes of mice, with males exhibiting higher neuronal activity during attack. Utilizing single-nucleus RNA sequencing, we characterized diverse landscape pSI neurons, revealing significant...
While aggressive behaviors are universal and essential for survival, ‘uncontrollable’ abnormal in animals or humans may have severe adverse consequences social costs. Neural circuits regulating specific forms of aggression under defined conditions been described, but whether brain governing a general response remains unknown. Here, we found that posterior substantia innominata (pSI) neurons responded to multiple aggression-provoking cues with the graded activity differential dynamics,...
Male animals often display higher levels of aggression than females, yet the neural circuit mechanism that is responsible for sexually dimorphic remains elusive. Here, we identify a hypothalamic-amygdala mediates male-biased in mice. Specifically, ventrolateral part ventromedial hypothalamus (VMHvl), region associated with aggression, densely projects to posterior substantia innominata (pSI), which promotes similar attack both sexes Notably, VMHvl unidirectionally innervates pSI through...
SUMMARY While aggressive behaviors are universal and essential for survival, ‘uncontrollable’ abnormal in animals or humans may have severe adverse consequences social costs. Neural circuits regulating specific forms of aggression under defined conditions been described, but how brain govern a general response remains unknown. Here, we found that posterior substantia innominata (pSI) neurons responded to several aggression-provoking cues with the graded activity differential dynamics,...