Lia et al. [1] discovered the critical role of STIM1 ER Ca sensor in the functional decline of astrocytes in the AD-like pathology in PS2APP mice. Profound downregulation of STIM1 expression in astrocytes in the disease results in the decreased ER Ca content and severely impaired evoked as well as spontaneous astrocytic Ca signalling. Aberrant astrocytic Ca signalling translated into impaired synaptic plasticity and memory. Astrocyte-specific overexpression of STIM1 restored Ca excitability and rectified synaptic and memory deficits.
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http://dx.doi.org/10.1016/j.ceca.2023.102756 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.
Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). Recent studies have identified a population of disease-associated astrocytes (DAA)-like astrocytes closely linked to amyloid deposition and tau pathology in an AD mouse model. However, the presence and role of these astrocytes in high-salt diet (HSD) models remain unexplored.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Department of Neurology, Mental and Neurological Disease Research Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Aims: The aim of this study is to investigate the role of glymphatic function of cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL), the most common monogenic small vessel disease caused by NOTCH3 mutation, and to explore potential therapeutic strategies to improve glymphatic function.
Methods: We assessed glymphatic influx and efflux function in CADASIL mouse models (Notch3) and correlated these findings with brain atrophy in CADASIL patients. We also investigated the underlying mechanisms of glymphatic impairment, focusing the expression of AQP4 in astrocytic endfeet.
Curr Issues Mol Biol
December 2024
Immunology Research Lab & BK21-Four Educational Research Group for Age-Associated Disorder Control Technology, Department of Biological Science, Chosun University, Gwangju 61452, Republic of Korea.
Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, and disease. While acute neuroinflammation plays a protective role by facilitating pathogen clearance and tissue repair, chronic and dysregulated inflammation contributes significantly to the progression of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Multiple Sclerosis. This review explores the cellular and molecular mechanisms underlying neuroinflammation, focusing on the roles of microglia, astrocytes, and peripheral immune cells.
View Article and Find Full Text PDFBrain Sci
January 2025
Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Charcot first described ALS in 1869, but the specific mechanisms that mediate the disease pathology are still not clear. Intense research efforts have provided insight into unique neuroanatomical regions, specific neuronal populations and genetic associations for ALS and other neurodegenerative diseases; however, the experimental results also suggest a convergence of these events to common toxic pathways. We propose that common toxic pathways can be therapeutically targeted, and this intervention will be effective in slowing progression and improving patient quality of life.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Background: Acupoint catgut embedding (ACE) is a traditional Chinese medicine technique commonly used for managing various disorders, including chronic inflammatory pain and allergic asthma. Despite its growing use, the neuroimmunological mechanisms underlying ACE treatment effects remain unclear.
Methods: This study investigated the roles and potential mechanisms of the effects of ACE in treating experimental autoimmune encephalomyelitis (EAE), a frequently used animal model of autoimmune neuroinflammation.
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