ArticleJournal of Alzheimer's disease : JAD2018
A Study of Amyloid-β and Phosphotau in Plaques and Neurons in the Hippocampus of Alzheimer's Disease Patients.
Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Increased expression of inflammasome signaling genes and proteins in selective brain regions in the intermediate stage of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- Development of a Novel AAV-Mediated microRNA Gene Therapy for Spatial Suppression of BACE1 to Improve Cognitive Function in Alzheimer's Disease Model Mice.Biomolecules · 2026Article
- Amyloid-β aggregates induce vasculopathy via ferroptosis in brain endothelial cells.Brain pathology (Zurich, Switzerland) · 2026Article
- Comparative Evaluation of Imatinib and Nilotinib in a Streptozotocin-Induced Rat Model of Alzheimer's Disease : Neuroprotective, Anti-inflammatory, and Cognitive Outcomes.Journal of Korean Neurosurgical Society · 2026Article
- Genetics of educational resilience after adverse childhood experiences.EBioMedicine · 2026Article
- Erythrocyte Load in Cerebrospinal Fluid Linked with Hippocampal Atrophy in Alzheimer's Disease.Journal of clinical medicine · 2025Article
- Promising Strategies to Reduce the SARS-CoV-2 Amyloid Deposition in the Brain and Prevent COVID-19-Exacerbated Dementia and Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Three-dimensional histology reveals dissociable human hippocampal long-axis gradients of Alzheimer's pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Pharmacological enhancement of cholinergic neurotransmission alleviates neuroinflammation and improves functional outcomes in a triple transgenic mouse model of Alzheimer's disease.Frontiers in pharmacology · 2024Article
- Corpora amylacea negatively correlate with hippocampal tau pathology in Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Three-dimensional histology reveals dissociable human hippocampal long axis gradients of Alzheimer's pathology.bioRxiv : the preprint server for biology · 2023Article
- Aberrant accumulation of age- and disease-associated factors following neural probe implantation in a mouse model of Alzheimer's disease.Journal of neural engineering · 2023Article
- Identification of inflammasome signaling proteins in neurons and microglia in early and intermediate stages of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2023Article
- Profiling neuroprotective potential of trehalose in animal models of neurodegenerative diseases: a systematic review.Neural regeneration research · 2023Review
- Transfusion with Blood Plasma from Young Mice Affects rTg4510 Transgenic Tau Mice Modeling of Alzheimer's Disease.Brain sciences · 2023Article
- 8-Hydroxyquinolylnitrones as multifunctional ligands for the therapy of neurodegenerative diseases.Acta pharmaceutica Sinica. B · 2023Article
- Functional excitatory to inhibitory synaptic imbalance and loss of cognitive performance in people with Alzheimer's disease neuropathologic change.Acta neuropathologica · 2023Article
- SARS-CoV-2 amyloid, is COVID-19-exacerbated dementia an amyloid disorder in the making?Frontiers in dementia · 2023Article
- Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies.Journal of visualized experiments : JoVE · 2022Article
- Are mitophagy enhancers therapeutic targets for Alzheimer's disease?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
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3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main pathological hallmarks in Alzheimer's disease (AD) are the presence of extracellular amyloid plaques, primarily consisting of amyloid-β (Aβ) peptide, and the accumulation of paired helical filaments of hyperphosphorylated tau protein (PHF-Tau) within neurons. Since CA1 is one of the most affected regions in AD, mainly at early stages, we have performed a detailed analysis of the CA1 region from 11 AD patients (demented and clinically similar; Braak stages IV-VI) to better understand the possible relationship between the presence and distribution of different neurochemical types of Aβ plaques and PHF-Tau immunoreactive (- ir) neurons. Hence, we have examined hippocampal sections in confocal microscopy images from double and triple-immunostained sections, to study labeled plaques and PHF-Tau-ir neurons using specific software tools. There are four main findings in the present study. First, the pyramidal layer of proximal CA1 (close to CA2) contains the smallest number of both plaques and PHF-Tau-ir neurons. Second, a large proportion of Aβ-ir plaques were also characterized by the presence of PHF-Tau-ir. Third, all plaques containing one of the two PHF-Tau isoforms also express the other isoform, that is, if a plaque contains PHFpS396, it also contains PHFAT8, and vice versa. Fourth, the coexpression study of both PHF-Tau isoforms in CA1 neurons revealed that most of the labeled neurons express only PHFpS396. Our findings further support the idea that AD is not a unique entity even within the same neuropathological stage, since the microanatomical/neurochemical changes that occur in the hippocampus greatly vary from one patient to another.
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