ReviewBrain pathology (Zurich, Switzerland)2016
Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease.
Review in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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
49 citing papers in PubMed, 76 citations in OpenAlex.
- Dysregulated TIE-2 expression is associated with blood-brain barrier leakiness and Alzheimer's disease-related neuropathology.Brain pathology (Zurich, Switzerland) · 2026Article
- Calcium dysregulation in neurovascular function in Alzheimer's disease: mechanisms, therapeutic targets.GeroScience · 2026Review
- Article
- Cardiometabolic risk mediates the association between perceived stress and learning and memory similarly among Hispanic/Latino and non-Hispanic White individuals.Journal of clinical and experimental neuropsychology · 2026Observational
- Linking EEG markers of oscillopathy and default mode network dysfunction in Alzheimer's disease.Frontiers in human neuroscience · 2026Review
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Exploring the effect of pre-clinical Alzheimer's disease on blood pressure using Mendelian randomisation and parental dementia as an instrumental variable in UK Biobank.BMC medicine · 2025Article
- Alterations in cerebral perfusion and substrate metabolism in type 2 diabetes: interactions with APOE-ε4.Diabetologia · 2025Article
- Exercise-mediated cerebrovascular repair in Alzheimer's disease: from pathophysiology to therapeutic precision.Frontiers in aging neuroscience · 2025Review
- Potential Roles of Hypoxia-Inducible Factor-1 in Alzheimer's Disease: Beneficial or Detrimental?Antioxidants (Basel, Switzerland) · 2024Review
- Alzheimer's Disease: Understanding Motor Impairments.Brain sciences · 2024Review
- The Cerebrovascular Side of Plasticity: Microvascular Architecture across Health and Neurodegenerative and Vascular Diseases.Brain sciences · 2024Review
- Prospective Longitudinal Perfusion in Probable Alzheimer's Disease Correlated with Atrophy in Temporal Lobe.Aging and disease · 2024Article
- Enhancing cognitive function in older adults: dietary approaches and implications.Frontiers in nutrition · 2024Review
- Overexpression of ACE2 ameliorates Aβ-induced blood-brain barrier damage and angiogenesis by inhibiting NF-κB/VEGF/VEGFR2 pathway.Animal models and experimental medicine · 2023Article
- Relationships between quantitative retinal microvascular characteristics and cognitive function based on automated artificial intelligence measurements.Frontiers in cell and developmental biology · 2023Article
- Decreased myelin proteins in brain donors exposed to football-related repetitive head impacts.Brain communications · 2023Article
- Elevated late-life blood pressure may maintain brain oxygenation and slow amyloid-β accumulation at the expense of cerebral vascular damage.Brain communications · 2023Article
- A Study on the Pathogenesis of Vascular Cognitive Impairment and Dementia: The Chronic Cerebral Hypoperfusion Hypothesis.Journal of clinical medicine · 2022Review
- Serum Neurofilament Light is elevated in COVID-19 Positive Adults in the ICU and is associated with Co-Morbid Cardiovascular Disease, Neurological Complications, and Acuity of Illness.Cardiology and cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
There is a perfusion deficit in Alzheimer's disease (AD), commencing in the precuneus and spreading to other parts of the cerebral cortex. The deficit anticipates the development of dementia, contributes to brain damage, and is caused by both functional and structural abnormalities of the cerebral vasculature. Most of the abnormalities are probably secondary to the accumulation of Aβ but the consequent hypoperfusion may, in turn, increase Aβ production. In the early stages of disease, abnormalities that cause vasoconstriction predominate. These include cholinergic vascular denervation, inhibition of endothelial nitric oxide synthase, increased production of endothelin-1 production and possibly also of angiotensin II. Patients with AD also have an increased prevalence of structural disease of cerebral microvessels, particularly CAA and capillary damage, and particularly in the later stages of disease these are likely to make an important contribution to the cerebral hypoperfusion. The metabolic abnormalities that cause early vascular dysfunction offer several targets for therapeutic intervention. However, for intervention to be effective it probably needs to be early. Prolonged cerebral hypoperfusion may induce compensatory circulatory changes that are themselves damaging, including hypertension and small vessel disease. This has implications for the use of antihypertensive drugs once there is accumulation of Aβ within the brain.
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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.