Skip to content
Open access

Mitochondrial dysfunction as a hallmark of brain senescence in telomerase-deficient mice

Aug 2026 · bioRxiv · 0 citations · 51 references
Biology

TL;DR

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.

Read PDF

Similar papers

Review Aug 2026

The organellar biology of aging: A mitochondrial vantage

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.

Madhusmita Pala, Abinash Nayak, Bandita Rath · 0 citations
Review Aug 2026

Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Therapeutic Advances.

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. · 0 citations
Review Open access Sep 2026

Rethinking Senescence Hallmarks in the Brain: Lessons From Peripheral Tissues and Challenges in Defining Neuronal Senescence

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 · 0 citations
Open access Sep 2026

Mitochondrial dysfunction and impaired osteogenic capacity define stress-induced osteoblast senescence

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. · 0 citations
Review 2026

Energetic crisis, mitochondrial vulnerability and disruption of lactate shuttle in Alzheimer's disease.

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 · 2 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.