2026· International review of neurobiology· Vol 188, pp.
299-361
· 0 citations
Medicine
TL;DR
This chapter looks at the nature of the tau-mitochondrial interface, and proposes a paradigm of tau-induced energy failure in AD, and discusses novel therapeutic approaches that target both tau and mitochondrial abnormalities, namely antisense oligonucleotides (ASO), mitochondria targeted compounds and mitophagy modifiers.
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
The roles of mitochondrial calcium uniporter (MCU) complex and mitochondrial sodium – calcium – lithium exchanger (NCLX) in regulating mitochondrial Ca²⁺ along with the therapeutic effects of regulating mitochondrial Ca²⁺ in the brain are highlighted.
Sahishnu Saha· American Journal of Student...· 0 citations
Findings support a model in which tau dysfunction results from the convergence of molecular aberrations and genetic susceptibility within a pathological network involving amyloid-β, neuroinflammation, and synaptic failure.
S. Sura, S. Jagadeesan, M. A. M. Moklas et al.· Molecular Biology Reports· 0 citations
A novel interpretation of the aging-related pathogenic mechanisms of AD from a mitochondrial perspective is provided, a theoretical foundation for the development of precise and efficient mitochondria-targeted therapeutic strategies for AD is laid, and a new paradigm for breaking through the bottlenecks of clinical dia...
Xiong Li, Rui Wan, Yu-Meng Wu et al.· Ageing Research Reviews· 0 citations
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