Cerebrovascular resistance: effects on cognitive decline, cortical atrophy, and progression to dementia
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See Markus (doi:10.1093/awx161) for a scientific commentary on this article.Evidence for vascular contributions to Alzheimer's disease has been increasingly identified, with increased blood pressure and decreased cerebral blood flow both linked to in vivo biomarkers and clinical progression of Alzheimer's disease. We therefore hypothesized that an elevated ratio of blood pressure to cerebral blood flow, indicative of cerebrovascular resistance, would exhibit earlier and more widespread associations with Alzheimer's disease than cerebral blood flow alone. Further, we predicted that increased cerebrovascular resistance and amyloid retention would synergistically influence cognitive performance trajectories, independent of neuronal metabolism. Lastly, we anticipated associations between cerebrovascular resistance and later brain atrophy, prior to amyloid accumulation. To evaluate these hypotheses, we investigated associations between cerebrovascular resistance and amyloid retention, cognitive decline, and brain atrophy, controlling for neuronal metabolism. North American older adults (n = 232) underwent arterial spin labelling magnetic resonance imaging to measure regional cerebral blood flow in brain regions susceptible to ageing and Alzheimer's disease. An estimated cerebrovascular resistance index was then calculated as the ratio of mean arterial pressure to regional cerebral blood flow. Positron emission tomography with 18F-florbetapir and fludeoxyglucose was used to quantify amyloid retention and neuronal metabolism, respectively. Cognitive performance was evaluated via annual assessments of global cognition, memory, and executive function. Results indicated diminished inferior parietal and temporal cerebral blood flow for patients with Alzheimer's disease (n = 33) relative to both non-demented groups, but no cerebral blood flow differences between non-demented amyloid-positive (n = 87) and amyloid-negative (n = 112) cases. In contrast, the cerebrovascular resistance index was significantly elevated in amyloid-positive versus amyloid-negative cases, with additional elevation in patients with Alzheimer's disease. Furthermore, cerebrovascular resistance index group differences were of greater statistical effect size and encompassed a greater number of brain regions than those for cerebral blood flow alone. Cognitive decline over 2-year follow-up was accelerated by elevated baseline cerebrovascular resistance index, particularly for amyloid-positive individuals. Increased baseline cerebrovascular resistance index also predicted greater progression to dementia, beyond that attributable to amyloid-positivity. Finally, increased cerebrovascular resistance index predicted greater regional atrophy among non-demented older adults who were amyloid-negative. Findings suggest that increased cerebrovascular resistance may represent a previously unrecognized contributor to Alzheimer's disease that is independent of neuronal hypometabolism, predates changes in brain perfusion, exacerbates and works synergistically with amyloidosis to produce cognitive decline, and drives amyloid-independent brain atrophy during the earliest stage of disease.
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Amyloid-induced vascular constriction, increased vascular resistance, and degeneration of pericytes may further contribute to hypoperfusion.
“Amyloid-induced vascular constriction, increased vascular resistance, and degeneration of pericytes may further contribute to hypoperfusion (Kisler et al., 2017; Yew et al., 2017).”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Yew et al., 2017
The Introduction (page unavailable) says amyloid-induced vasoconstriction can increase cerebrovascular resistance, and the Discussion links vascular resistance changes with reduced cerebral blood flow. The cited paper does not address pericyte degeneration, so it supports only part of the attributed claim. (LLM, conf=0.87)
Experimental — accuracy not yet measuredVascular alterations such as cerebrovascular resistance and hypoperfusion may precede amyloid deposition and are predictive of future disease progression.
“In support of this hypothesis, recent evidence from neuroimaging studies suggests that vascular alterations such as cerebrovascular resistance and hypoperfusion may precede amyloid deposition and are predictive of future disease progression (Iturria-Medina et al., 2016; Yew et al., 2017).”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Yew et al., 2017
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White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease
Araque Caballero, M. Á., Suárez-Calvet, M., Duering, M., Franzmeier, N., Benzinger, T., Fagan, A. M., Bateman, R. J., Jack, C. R., Levin, J., Dichgans, M., et al. (2018) · Brain · doi:10.1093/brain/awy229 · Cited by 179 · see citing works
Calderón-Garcidueñas, L., González-Maciel, A., Reynoso-Robles, R., Kulesza, R. J., Mukherjee, P. S., Torres-Jardón, R., Rönkkö, T., & Doty, R. L. (2018) · Environmental Research · doi:10.1016/j.envres.2018.06.027 · Cited by 110 · see citing works
- Authors
- Yew, B., Nation, D. A., & Initiative, F. T. A. D. N.
- Affiliations
- University of Southern California (US)
- ORCID
- Nation, Daniel A.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-06-01
- Volume
- 140
- Issue
- 7
- Pages
- 1987-2001
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC6059092
- OpenAlex
- W2621215132
- Cited by
- 133
- References
- 76
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 11 · 2023: 12 · 2022: 19 · 2021: 31 · 2020: 16 · 2019: 12 · 2018: 9 · 2017: 6
- FWCI
- 9.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIH (P50 AG005142, P01 AG052350)
- Foundation for the National Institutes of Health
- National Institutes of Health (U01 AG024904, W81XWH-12-2-0012)
- National Institute on Aging
- National Institute of Biomedical Imaging and Bioengineering
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- cerebrovascular resistance, Alzheimer's disease, cognitive decline, dementia progression, cerebral blood flow, cortical atrophy, arterial spin labeling, 18F-florbetapir, blood pressure, older adults, brain aging
- MeSH terms
- Aged, Alzheimer Disease, Amyloid, Aniline Compounds, Atrophy, Blood Pressure, Brain, Cerebral Cortex, Ethylene Glycols, Female, Humans, Magnetic Resonance Imaging, Male, Neurons, Neuropsychological Tests, Spin Labels, Vascular Resistance, Disease Progression, Fluorodeoxyglucose F18, Positron-Emission Tomography, Neuroimaging, Cognitive Dysfunction, White Matter
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