ReviewActa neuropathologica2020
Cerebral blood flow decrease as an early pathological mechanism in Alzheimer's disease.
Review in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 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.
The trial behind it
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
206 citing papers in PubMed, 340 citations in OpenAlex.
- The Impact of Cocoa Flavanols in Modulating Resting Cerebral Blood Flow During Prolonged Sitting in Healthy Young and Older Adults.Nutrients · 2025Trial
- Exploring the effect of multi-modal intervention against cognitive decline on atrophy and small vessel disease imaging markers in the AgeWell.de imaging study.NeuroImage. Clinical · 2025Trial
- NeuroEPO plus (NeuralCIMAlzheimer's research & therapy · 2023Trial
- Trial
- Cognitive Effects of the BET Protein Inhibitor Apabetalone: A Prespecified Montreal Cognitive Assessment Analysis Nested in the BETonMACE Randomized Controlled Trial.Journal of Alzheimer's disease : JAD · 2021Trial
- PTUPB improves cognitive function in Alzheimer's disease associated with enhancing cerebral vascular myogenic response and attenuating vascular remodeling.GeroScience · 2026Article
- Review
- Neuroinflammatory and molecular pathways in Alzheimer's disease: mechanistic crosstalk and emerging therapeutic opportunities.Inflammopharmacology · 2026Review
- Calcium dysregulation in neurovascular function in Alzheimer's disease: mechanisms, therapeutic targets.GeroScience · 2026Review
- Cerebral Intramural Cells: A Missing Cellular Link Between Vascular Aging and Alzheimer's Disease.International journal of molecular sciences · 2026Review
- The Associations of cerebral blood flow and white matter hyperintensities with tau and amyloid-beta across the Alzheimer's disease spectrum.Brain imaging and behavior · 2026Article
- Reduced Retinal Perfusion With Preserved Microvascular Network Density in Early Alzheimer's Disease: A Multimodal Imaging Study.Translational vision science & technology · 2026Article
- Sleep apnea in REM sleep as an amplifier of vascular contributions to Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- The mechanisms and strategies for Alzheimer's disease prevention: An update.Acta pharmaceutica Sinica. B · 2026Review
- Glycocalyx and basal lamina in neurological disorders.Matrix biology : journal of the International Society for Matrix Biology · 2026Review
- The Associations of Cerebral Blood Flow and White Matter Hyperintensities with Tau and Amyloid-beta Across the Alzheimer's Disease Spectrum.medRxiv : the preprint server for health sciences · 2026Article
- Chemogenetic modulation of CNS pericytes: Impact on pericyte CaMolecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Vessel-associated microglia are differentially activated and distributed in relation to systemic infection and Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- Multi-parametric longitudinal imaging of cerebral biomarkers in a rodent model of Alzheimer's disease.Photoacoustics · 2026Article
- Brain network dynamics determine tau presence while regional vulnerability governs tau load in Alzheimer's disease.Research square · 2026Article
146 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Therapies targeting late events in Alzheimer's disease (AD), including aggregation of amyloid beta (Aβ) and hyperphosphorylated tau, have largely failed, probably because they are given after significant neuronal damage has occurred. Biomarkers suggest that the earliest event in AD is a decrease of cerebral blood flow (CBF). This is caused by constriction of capillaries by contractile pericytes, probably evoked by oligomeric Aβ. CBF is also reduced by neutrophil trapping in capillaries and clot formation, perhaps secondary to the capillary constriction. The fall in CBF potentiates neurodegeneration by upregulating the BACE1 enzyme that makes Aβ and by promoting tau hyperphosphorylation. Surprisingly, therefore, CBF reduction may play a crucial role in driving cognitive decline by initiating the amyloid cascade itself, or being caused by and amplifying Aβ production. Here, we review developments in this area that are neglected in current approaches to AD, with the aim of promoting novel mechanism-based therapeutic approaches.
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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 Socratic graph.