Neurodegenerative diseases and their associated cognitive decline are known to be more prevalent during aging. Recent evidence has uncovered the role of microglia, the immunocompetent cells of the brain, in dysfunctions linked to neurodegenerative diseases such as is Alzheimer's disease (AD). Similar to other pathologies, AD is shown to be sex-biased, with females being more at risk compared to males. While the mechanisms driving this prevalence are still unclear, emerging data suggest the sex differences present in microglia throughout life might lead to different responses of these cells in both health and disease. Furthermore, microglial cells have recently been recognized as a deeply heterogeneous population, with multiple subsets and/or phenotypes stemming from diverse parameters such as age, sex or state of health. Therefore, this review discusses microglial heterogeneity during aging in both basal conditions and AD with a focus on existing sex differences in this process.
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http://dx.doi.org/10.1016/j.jphs.2021.03.006 | DOI Listing |
Demyelination, or the loss of myelin in the central nervous system (CNS) is a hallmark of multiple sclerosis (MS) and occurs in various forms of CNS injury and neurodegenerative diseases. The regeneration of myelin, or remyelination, occurs spontaneously following demyelination. The lysophosphatidylcholine (LPC)-induced focal demyelination model enables investigations into the mechanisms of remyelination, providing insight into the molecular basis underlying an evolving remyelinating microenvironment over a tractable time course.
View Article and Find Full Text PDFGlia
January 2025
Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA.
Human genetics studies lent firm evidence that microglia are key to Alzheimer's disease (AD) pathogenesis over a decade ago following the identification of AD-associated genes that are expressed in a microglia-specific manner. However, while alterations in microglial morphology and gene expression are observed in human postmortem brain tissue, the mechanisms by which microglia drive and contribute to AD pathology remain ill-defined. Numerous mouse models have been developed to facilitate the disambiguation of the biological mechanisms underlying AD, incorporating amyloidosis, phosphorylated tau, or both.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Department of Pharmacy, the Second Affiliated Hospital of Shaoyang University, Shaoyang, Hunan, China.
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) plaques and the aggregation of tau protein, resulting in intense memory loss and dementia. Diabetes-associated cognitive dysfunction (DACD) is a complication of diabetes mellitus, which is associated with decreased cognitive function and impaired memory. A growing body of literature emphasize the involvement of microglia in AD and DACD.
View Article and Find Full Text PDFFront Neurol
December 2024
The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Mol Med
December 2024
Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, 197 Ruijin er Road, Shanghai, 200025, China.
Background: Glaucoma is a group of heterogeneous neurodegenerative diseases with abnormal energy metabolism and imbalanced neuroinflammation in the retina. Thioredoxin-interacting protein (TXNIP) is involved in glucose and lipid metabolism, and associated with oxidative stress and inflammation, however, not known whether to be involved in glaucoma neuropathy and its underlying mechanisms.
Methods: To establish the chronic ocular hypertension (COH) mice model.
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