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Cited by 104Alzheimer's disease research and treatmentsBarrier Structure and Function StudiesNeurological Disease Mechanisms and Treatments

Neurovascular Pathways and Alzheimer Amyloid β-peptide

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Zlokovic, Berislav V., Deane, Rashid, Sallstrom, Jan, Chow, Nienwen, Miano, Joseph M.·2006·Brain Pathology
DOI 10.1111/j.1750-3639.2005.tb00103.xPMC PMC8095816
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Abstract

According to the prevailing amyloid cascade hypothesis, the onset and progression of a chronic neurodegenerative condition in Alzheimer disease (AD) is initiated by the amyloid beta-peptide (Abeta) accumulation in brain and consequent neuronal toxicity. Recent emphasis on co-morbidity of AD and cerebrovascular disease and the recognition that cerebrovascular dysregulation is an important feature of AD, has shed new light on neurovascular dysfunction as a possible contributor to cognitive decline and Alzheimer neurodegeneration. In the same time, this association has raised a question as to whether there is a causal relationship between cerebrovascular dysregulation and Abeta-initiated pathology, and whether influencing targets in the neurovasculature may prevent different forms of Abeta brain accumulation and/or lower pre-existing accumulates in a later stage of the disease. Pathogenic cascades which operate to dissociate normal transport exchanges between central and peripheral pools of Abeta, and decreased vascular competence leading to brain hypoperfusion and impaired Abeta clearance are discussed. We suggest that there is a link between neurovascular dysfunction and elevated brain Abeta which provides a new scenario for therapeutic interventions to control Alzheimer mental deterioration.

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Crossref · 10.1111/j.1750-3639.2005.tb00103.x

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  • apoE is synthesized mainly by astrocytes and plays an isoform-dependent role in modulating Aβ fibrillization and clearance.

    “apoE is synthesized mainly by astrocytes and plays an isoform-dependent role in modulating Aβ fibrillization and clearance (Holtzman, 2001; Zlokovic et al., 2005; Kim et al., 2009).”

    From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Zlokovic et al., 2005

    The matching passages are in the References section (page not provided): they list studies about apoE and Aβ metabolism or degradation, but do not state the claim as a finding of this paper. Searches for apoE, astrocytes, fibrillization, and apoE isoforms found no passage establishing that apoE is synthesized mainly by astrocytes or that its effects on Aβ fibrillization and clearance are isoform-dependent. (LLM, conf=0.72)

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Cited by

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Authors
Zlokovic, B. V., Deane, R., Sallstrom, J., Chow, N., & Miano, J. M.
Affiliations
  • Socratech (United States) (US)
  • University of Rochester Medicine (US)
ORCID
Venue
Brain Pathology
Publisher
Wiley
Published
2006-04-05
Volume
15
Issue
1
Pages
78-83
ISSN
1015-6305 (ISSN-L)
DOI
10.1111/j.1750-3639.2005.tb00103.x
PMC
PMC8095816
OpenAlex
W1978907821
Cited by
104
References
11
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 8 · 2021: 6 · 2020: 4 · 2019: 3 · 2018: 3 · 2017: 7 · 2016: 5 · 2015: 5 · 2014: 5 · 2013: 6 · 2012: 4
FWCI
1.09
Type
journal article
Language
en
Open access
Licence
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 3436 d)
Locations
  • Brain Pathology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1r43ag024002-01)
  • National Institute on Aging (AG024002, AG203993, AG023084)
  • National Heart, Lung, and Blood Institute (HL63290, R01HL063290)
  • National Institute of Neurological Disorders and Stroke (NS34467)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
Alzheimer's disease, amyloid-beta, amyloid hypothesis, neurovascular dysfunction, cerebrovascular disease, cerebral hypoperfusion, amyloid clearance, cognitive decline, therapeutic target
MeSH terms
Alzheimer Disease, Animals, Brain, Cerebrovascular Disorders, Humans, Models, Neurological, Amyloid beta-Peptides

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