ArticleBrain communications2025
Vulnerability of the entorhinal cortex II to neurodegeneration in Alzheimer's disease.
Article in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Limbic-Predominant Cortical Magnetic Susceptibility Alterations Are Associated With Glycemic Dysregulation and Cognitive Performance in Type 2 Diabetes.CNS neuroscience & therapeutics · 2026Article
- Comparative analysis of neuronal proteolytic pathways reveals neuron-specific and sub-compartmental-specific capacities with aging.Cellular and molecular life sciences : CMLS · 2026Article
- Post-translational modifications as a regulatory code for tau function in health and disease.Frontiers in dementia · 2026Review
- Peer review: a collective commitment to knowledge and excellence.Brain communications · 2026Article
- Linking dietary patterns to Alzheimer's disease biomarkers with network mathematical modeling could enable new approach methodologies in preventative AD research: a narrative interdisciplinary review.Frontiers in nutrition · 2025Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is characterized by progressive memory loss and deterioration of cognitive functions. The presence of neurofibrillary tangles in the hippocampal areas (perforant pathway) correlates with cognitive impairment. Pathological processing of tau protein is characterized by post-translational changes such as hyperphosphorylation and truncation, which favour conformational changes within tau. These conformational changes can be regional (dependent on phosphorylation) or structural (depending on regional conformational changes and truncation). Through immunohistochemical and immunofluorescence staining in hippocampus Alzheimer disease brains and quantification in tissue stained with TG3 antibody and analysed by confocal microscopy, we have been able to demonstrate that TG3 correlates with cognitive impairment. In the process of tangle evolution, TG3 is present in pre-tangle. This epitope of the TG3 antibody was very stable to proteolytic processing by caspase-3; truncation is evidenced by the TauC-3 antibody. The entorhinal cortex showed high sensitivity to neurodegeneration and pathological tau processing.
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Registered trials
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