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Neural ageing is the process by which neural cells in the brain and peripheral nervous system deteriorate structurally and functionally over time. It is associated with a decline in sensory, motor and cognitive functions of the brain.
Partially reprogramming a specific population of neurons in the cerebral cortex of mice, improves cognition through greater activation in memory circuits and plasticity induced by the reorganization of the extracellular matrix.
Identifying modifiable risk factors that could prevent depression is important. Here, the authors show increased risks of incident depression in pre-frail and frail individuals and highlight the mediating role of brain structure and inflammation.
Human glial progenitor cells (hGPCs) lose mitotic competence with age. Here, the authors show that with maturation, adult hGPCs acquire a set of transcriptional repressors that actively suppress developmental gene expression.
How synapses at dendrites are organized to optimize information processing remains elusive. Here, the authors found that intracellular magnesium optimizes transmission, plasticity, and coding capacity of synapses by reconfiguring their connectivity at dendrites.
In mice, a subset of neurons in the dorsomedial hypothalamus control sympathetic nervous system signalling to adipose tissue and are dysregulated with age; activating these neurons prolongs lifespan and slows the decline in physical activity associated with ageing.
Around 10% of individuals with frontotemporal lobar dementia have amyloid filament inclusions that lack tau and TDP-43 and were thought to contain the protein FUS, but are found instead to contain the FUS homologue TAF15.
Senescent cells in the brain contribute to age-related neurodegeneration. Analysis of SARS-CoV-2 infection in human brain organoids, animals and post-mortem brain samples from patients with COVID-19 reveals virus-induced senescence. Pharmacological senolytic treatment following SARS-CoV-2 infection improves COVID-19 neuropathology and could help to protect people from long COVID.
Neuronal aging is highly associated with misfolded protein aggregates that predispose to neurodegeneration, but the cellular factors that are involved in removing misfolded proteins are yet to be identified. In this issue of Nature Aging, Li and colleagues identified LONRF2 as an important player in protecting aging neurons against the accumulation of protein aggregates.
The number of neural stem cells in the brain decreases with age, which in the dentate gyrus of older mice is associated with a lower SIRT7-mediated mitochondrial unfolded protein response and reduced neural stem cell maintenance and neurogenesis.