A major consequence of telomere dysfunction associated with pathological brain aging is the downregulation of mitochondrial activity, which contributes to the selective vulnerability of specific brain regions, highlighting mitochondrial pathways as attractive targets for interventions aimed at preserving brain health during aging.
More research in the field may unravel the mechanistic details of the organellar crosstalk that works in concert with classical aging pathways to sustain aging progression, which may help promote healthier aging.
It is demonstrated that mitochondrial impairment precedes classical neuropathological hallmarks, thereby positioning mitochondrial dysfunction as a primary driver rather than a secondary consequence of neurodegeneration, and critically evaluates the translational landscape of mitochondria-targeted interventions.
Zhaomin Yao, Yang-Wa Wei, Weiming Xie et al.· Ageing Research Reviews· 0 citations
How cell type, inducing stressor, and experimental context shape senescence‐associated phenotypes across neural systems, including in vitro models, physiologically aged brains, and models of Alzheimer's and Parkinson's disease is examined.
Miraj Ud Din Momand, Kristina Macova, Dominika Fricova· Aging Cell· 0 citations
Cellular senescence has emerged as a key contributor to age-related skeletal deterioration; however, the defining characteristics of senescent osteoblasts remain incompletely understood, hindering efforts to identify the cellular mechanisms that drive age-associated bone loss and potential therapeutic targets. Here, we...
Tanja Frey, Hannah Vogg, Mubashir Ahmad et al.· bioRxiv· 0 citations
Cerebral bioenergetic metabolic failure as a central driver of cognitive decline, arising from irreversible reactive gliosis and neuroblastosis mechanisms is emphasised and various therapeutic options are highlighted, including restoration of ANLS to mitigate the pathogenesis and memory loss in AD.
Gowsika Baskar, Mahesh Kandasamy· International review of neur...· 2 citations
A mechanism by which aging reduces autophagic flux secondary to a loss of neuritic lysosomes, resulting in mitochondria-intrinsic mechanisms to avoid loss of energy production is revealed.
Eva Klinman, Ji-sun Kwon, Roland E. Dolle et al.· Autophagy· 0 citations
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