Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer's disease.

Mitochondrial homeostasis dysregulation: Potential mechanisms of Alzheimer's disease mediated by TDP-43.

Key features of mitochondrial homeostasis in neurons are outlined, neuropathological and clinical data supporting the relevance of TDP-43 in AD are reviewed, and emerging mechanisms by which TDP-43 may perturb mitochondrial homeostasis are synthesized.

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.

The Tau-mitochondria connection and its impact on cellular energy metabolism in Alzheimer's disease.

Autophagy-lysosomal pathway in neurodegeneration

Dysregulation of ALP-associated processes, including autophagic flux, chaperone-mediated autophagy, endolysosomal trafficking, lysosomal pH and ion balance, and lysosomal metabolic signaling, is implicated in both the pathogenesis and progression of neurodegenerative diseases, with an emphasis on Alzheimer’s disease an...

Multi‐Omics Analysis Reveals That Aβ42‐ Me3 Co‐Aggregation Induces Mitophagy Blockade in Early Stages of Alzheimer's Disease

Mitochondrial dysfunction is one of the earliest pathological features of Alzheimer's disease (AD), preceding overt neurodegeneration and cognitive decline. Amyloid‐β (Aβ) accumulation has long been considered a central pathogenic event in AD, yet how Aβ toxicity is mechanistically linked to mitochondrial impairment du...

Mitochondrial Calcium Dysregulation: A Central Nexus in Alzheimer’s Disease Pathogenesis and Therapeutic Intervention

Research in Alzheimer’s disease (AD) has been primarily focused on the genetic causes and therapies to target the amyloid‑β (Aβ) plaques and neurofibrillary tau tangles (NFTs). However, a growing body of research suggests that imbalances and subsequent breakdown in mitochondrial calcium (Ca²⁺) regulation plays a centra...