Archives
International Journal of Zoology and Applied Biosciences Research Article
Pathological consequences of Tau hyperphosphorylation in Alzheimer’s disease
Kiran Kumar S, Senthilkumar G P, Dhilip kumar P, Thiruselvi S and Chandra Lekha S B
Year : 2025 | Pages: 155-158
Received on: 18/09/2025
Revised on: 20/10/2025
Accepted on: 28/10/2025
Published on: 15/11/2025
-
Kiran Kumar S, Senthilkumar G P, Dhilip kumar P, Thiruselvi S and Chandra Lekha S B ( 2025).
Pathological consequences of Tau hyperphosphorylation in Alzheimer’s disease
. International Journal of Zoology and Applied Biosciences, 10( 6), 155-158.
-
click to view the cite format
Abstract
Tau hyperphosphorylation is a defining pathological hallmark of Alzheimer’s disease (AD), contributing directly to microtubule destabilization, synaptic failure, and neuronal degeneration. Under physiological conditions, tau stabilizes neuronal microtubules; however, excessive phosphorylation by kinases such as GSK-3β, CDK5, and MAPKs disrupts this function, promoting tau aggregation into neurofibrillary tangles (NFTs). This review synthesizes current evidence on the molecular mechanisms, cellular consequences, and neuropathological outcomes associated with hyperphosphorylated tau. Key findings highlight its involvement in impaired axonal transport, mitochondrial dysfunction, neuroinflammation, and widespread cortical atrophy. The paper also emphasizes emerging therapeutic approaches targeting tau phosphorylation pathways. Understanding the multifaceted pathological consequences of tau hyperphosphorylation is crucial for developing effective AD therapeutics.
Keywords
Tau protein, Hyperphosphorylation, Alzheimer’ s disease, Neurofibrillary tangles, GSK-3β .
-
Full Article PDF (
21)
- View HTML Article
Copy Rights
© The Author(s) 2025. This article is published by International Journal of Zoology and Applied Biosciences under the terms of the Creative Commons Attribution 4.0 International License (creativecommons.org), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
