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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.
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.
How excitatory neurons (EN) acquire senescence is unclear. Here, the authors show that GDF11 in ENs slows EN senescence, brain ageing, cognitive decline and maintains lifespan, revealing a mechanism underlying EN senescence and brain ageing.
Aguado et al. show that SARS-CoV-2 induces senescence in human brain organoids and in the brains of COVID-19-infected mice and humans. They demonstrate the therapeutic potential of senolytic therapy in protection against COVID-19-induced brain aging.
The mechanisms that underlie cognitive resilience during aging are poorly understood. Here, the authors describe a neurodegeneration checkpoint response mediated by the transcription factor REST that protects against the onset of Alzheimer’s disease.
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.
Combining high-throughput fluorescence-activated cell sorting and single-cell RNA sequencing, neurons with and without neurofibrillary tangles from people with Alzheimer disease were shown to have different molecular signatures.
