ArticleFrontiers in aging neuroscience2022
Ischemia as a common trigger for Alzheimer's disease.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Dietary diversity and cognitive performance in older adults: a systematic review.BMC neurology · 2025Pooled it
- Review
- Polyphenolic Imidazopyridines as Multifunctional Modulators of Oxidative Stress, Metal Dyshomeostasis, and βAntioxidants (Basel, Switzerland) · 2026Article
- The Role of Sphingosine-1-Phosphate Signaling in Cerebral Ischemia/Reperfusion Injury and Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- Phantom- and simulation-based validation of combined diffusion relaxometry in ex vivo ADRD white matter.bioRxiv : the preprint server for biology · 2026Article
- Drinking water arsenic, urinary arsenic biomarkers, and cognitive impairment in the REGARDS study.Environmental research · 2026Article
- 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
- Hyperbaric Oxygen Therapy for Cognitive Impairment Resulting from Neurological Disorders: Mechanisms of Action and Application Advances.International journal of medical sciences · 2026Review
- 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
- Statins in Acute Ischemic Stroke: Mechanisms, Resistance, and Precision Strategies for Neurovascular and Cognitive Protection.CNS drugs · 2025Review
- Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease.Brain sciences · 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 Potential Regulators of Amyloidogenic Pathway of APP Processing in Alzheimer's Disease.Biomedicines · 2025Review
- The Combination of Two Small Molecules Improves Neurological Parameters and Extends the Lifespan of C3H Strain Female Mice.Brain and behavior · 2025Article
- Exploring α-Syn's Functions Through Ablation Models: Physiological and Pathological Implications.Cellular and molecular neurobiology · 2025Review
- Do microglia metabolize fructose in Alzheimer's disease?Journal of neuroinflammation · 2025Review
- Differentially Expressed Genes in Rat Brain Regions with Different Degrees of Ischemic Damage.International journal of molecular sciences · 2025Article
- Vitamin K Properties in Stroke and Alzheimer's Disease: A Janus Bifrons in Protection and Prevention.Molecules (Basel, Switzerland) · 2025Review
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease has various potential etiologies, all culminating in the accumulation of beta -amyloid derivatives and significant cognitive decline. Vascular-related pathology is one of the more frequent etiologies, especially in persons older than 65 years, as vascular risk factors are linked to both cerebrovascular disease and the development of AD. The vascular patho-mechanism includes atherosclerosis, large and small vessel arteriosclerosis, cortical and subcortical infarcts, white matter lesions, and microbleeds. These insults cause hypoperfusion, tissue ischemia, chronic inflammation, neuronal death, gliosis, cerebral atrophy, and accumulation of beta-amyloid and phosphorylated tau proteins. In preclinical studies, hyperbaric oxygen therapy has been shown to reverse brain ischemia, and thus alleviate inflammation, reverse the accumulation of beta-amyloid, induce regeneration of axonal white matter, stimulate axonal growth, promote blood-brain barrier integrity, reduce inflammatory reactions, and improve brain performance. In this perspective article we will summarize the patho-mechanisms induced by brain ischemia and their contribution to the development of AD. We will also review the potential role of interventions that aim to reverse brain ischemia, and discuss their relevance for clinical practice.
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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.