ReviewCurrent Alzheimer research2024
A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model.
Review in Current Alzheimer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed.
- Article
- Dysfunctional respiration as a risk factor for Alzheimer disease: a hypothesis.Metabolic brain disease · 2026Review
- Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026Review
- The Role of Lipoprotein and Gut Microbiome in Alzheimer's Disease: A Review of Novel Findings and Potential Applications.Current Alzheimer research · 2026Review
- Quantitative Proteomic Analysis of APP/PS1 Transgenic Mice.Current Alzheimer research · 2026Article
- Alterations of Apolipoprotein A1, E, and J Genes in the Frontal Cortex in an Ischemic Model of Alzheimer's Disease with 2-Year Survival.International journal of molecular sciences · 2025Article
- Decoding Alzheimer's Disease: Single-Cell Sequencing Uncovers Brain Cell Heterogeneity and Pathogenesis.Molecular neurobiology · 2025Review
- Gender-Dependent Modulation of Alzheimer's Disease by Brain Ischemia. Comment on Lohkamp et al. Sex-Specific Adaptations in Alzheimer's Disease and Ischemic Stroke: A Longitudinal Study in Male and Female APPLife (Basel, Switzerland) · 2025Article
- The role of mitochondrial dysfunction in the pathogenesis of Alzheimer's disease and future strategies for targeted therapy.European journal of medical research · 2025Review
- Direct and indirect role of non-coding RNAs in company with amyloid and tau protein in promoting neuroinflammation in post-ischemic brain neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Topological Biomarkers of Alzheimer's Disease from Functional Brain Network Analysis.Current Alzheimer research · 2025Article
- Exploring the Role of Nutrition in Supporting Brain Health and Reducing the Risk of Alzheimer's Disease.Current Alzheimer research · 2025Review
- The Framework for an Integrative Theory of Alzheimer's Disease.Current Alzheimer research · 2025Review
- Alterations ofCurrent Alzheimer research · 2025Article
- Most prominent challenges in translational neuroscience and strategic solutions to bridge the gaps: Perspectives from an editorial board interrogation.Exploration of neuroscience · 2025Article
- Visualization Analysis of Tau Protein in the Brain of Alzheimer's Disease: A Scoping Literature Review.Current Alzheimer research · 2024Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the frequent form of dementia in the world. Despite over 100 years of research into the causes of AD, including amyloid and tau protein, the research has stalled and has not led to any conclusions. Moreover, numerous projects aimed at finding a cure for AD have also failed to achieve a breakthrough. Thus, the failure of anti-amyloid and anti-tau protein therapy to treat AD significantly influenced the way we began to think about the etiology of the disease. This situation prompted a group of researchers to focus on ischemic brain episodes, which, like AD, mostly present alterations in the hippocampus. In this context, it has been proposed that cerebral ischemic incidents may play a major role in promoting amyloid and tau protein in neurodegeneration in AD. In this review, we summarized the experimental and clinical research conducted over several years on the role of ischemic brain episodes in the development of AD. Studies have shown changes typical of AD in the course of brain neurodegeneration post-ischemia, i.e., progressive brain and hippocampal atrophy, increased amyloid production, and modification of tau protein. In the post-ischemic brain, the diffuse and senile amyloid plaques and the development of neurofibrillary tangles characteristic of AD were revealed. The above data evidently showed that after brain ischemia, there are modifications in protein folding, leading to massive neuronal death and damage to the neuronal network, which triggers dementia with the AD phenotype.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.