ArticlePloS one2023
Age-related changes in tau and autophagy in human brain in the absence of neurodegeneration.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Circulating pTau181 and Genomic Background in Dogs: A Pilot Study on Neurobiological Aging.Veterinary medicine international · 2026Article
- Estrogen Alleviates Sevoflurane-Induced Neurotoxicity by Inhibiting ERα-Tau Binding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The connection between autophagy and Alzheimer's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Review
- Cognitive capacity in amyotrophic lateral sclerosis: the value of diagnostic markers in cerebrospinal fluid and the influence of nutrition and pulmonary function.Brain communications · 2025Article
- Serum Oligomeric α-Synuclein and p-tau181 in Progressive Supranuclear Palsy and Parkinson's Disease.International journal of molecular sciences · 2024Article
- Astrocytic accumulation of tau fibrils isolated from Alzheimer's disease brains induces inflammation, cell-to-cell propagation and neuronal impairment.Acta neuropathologica communications · 2024Article
- Impaired biogenesis of basic proteins impacts multiple hallmarks of the aging brain.bioRxiv : the preprint server for biology · 2024Article
- Correlation of brain tissue volume loss with inflammatory biomarkers IL1β, P-tau, T-tau, and NLPR3 in the aging cognitively impaired population.Frontiers in aging neuroscience · 2024Article
- Nuclear face of Tau: an inside player in neurodegeneration.Acta neuropathologica communications · 2023Review
- Aging, NRF2, and TAU: A Perfect Match for Neurodegeneration?Antioxidants (Basel, Switzerland) · 2023Review
- Age-dependent accumulation of tau aggregation inFrontiers in aging · 2022Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tau becomes abnormally hyper-phosphorylated and aggregated in tauopathies like Alzheimers disease (AD). As age is the greatest risk factor for developing AD, it is important to understand how tau protein itself, and the pathways implicated in its turnover, change during aging. We investigated age-related changes in total and phosphorylated tau in brain samples from two cohorts of cognitively normal individuals spanning 19-74 years, without overt neurodegeneration. One cohort utilised resected tissue and the other used post-mortem tissue. Total soluble tau levels declined with age in both cohorts. Phosphorylated tau was undetectable in the post-mortem tissue but was clearly evident in the resected tissue and did not undergo significant age-related change. To ascertain if the decline in soluble tau was correlated with age-related changes in autophagy, three markers of autophagy were tested but only two appeared to increase with age and the third was unchanged. This implies that in individuals who do not develop neurodegeneration, there is an age-related reduction in soluble tau which could potentially be due to age-related changes in autophagy. Thus, to explore how an age-related increase in autophagy might influence tau-mediated dysfunctions in vivo, autophagy was enhanced in a Drosophila model and all age-related tau phenotypes were significantly ameliorated. These data shed light on age-related physiological changes in proteins implicated in AD and highlights the need to study pathways that may be responsible for these changes. It also demonstrates the therapeutic potential of interventions that upregulate turnover of aggregate-prone proteins during aging.
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