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The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.

Neurovascular mechanisms of Alzheimer's neurodegeneration

Zlokovic, Berislav V.·2005·Trends in Neurosciences
DOI 10.1016/j.tins.2005.02.001
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Abstract

In contrast to traditional neuroncentric views of Alzheimer's disease (AD), recent findings indicate that neurovascular dysfunction contributes to cognitive decline and neurodegeneration in AD. Here, I propose the neurovascular hypothesis of AD, suggesting that faulty clearance of amyloid beta peptide (A beta) across the blood-brain barrier (BBB), aberrant angiogenesis and senescence of the cerebrovascular system could initiate neurovascular uncoupling, vessel regression, brain hypoperfusion and neurovascular inflammation. Ultimately, this would lead to BBB compromise, to chemical imbalance in the neuronal environment and to synaptic and neuronal dysfunction, injury and loss. Based on the neurovascular hypothesis, I suggest an array of new potential therapeutic approaches that could be developed for AD, to enhance A beta clearance and neurovascular repair, and to protect the neurovascular unit from divergent inducers of injury and apoptosis.

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  • Low Aβ levels within the healthy brain are maintained through degradation, elimination via ISF bulk flow, CSF absorption into the circulatory and lymphatic system, or transport across the BBB.

    “Low Aβ levels within the healthy brain are maintained through degradation, elimination via interstitial fluid (ISF) bulk flow, cerebrospinal fluid (CSF) absorption into the circulatory and lymphatic system, or transport across the blood-brain barrier (BBB) (3,4).”

    From Endothelial LRP1 transports amyloid-β1–42 across the blood-brain barrier (2015) · cites this paper as [3]

  • The neurovascular hypothesis of AD states that Aβ accumulation is driven by impairment of Aβ transporters in brain capillaries, resulting in deficient Aβ elimination via the BBB.

    “Thus, the neurovascular hypothesis of AD states that Aβ accumulation is driven by impairment of Aβ transporters in brain capillaries, resulting in deficient Aβ elimination via the BBB (3,8,15,16).”

    From Endothelial LRP1 transports amyloid-β1–42 across the blood-brain barrier (2015) · cites this paper as [3]

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Metadata

Authors
Zlokovic, B. V.
Venue
Trends in Neurosciences
Publisher
Elsevier BV
Published
2005-04
Volume
28
Issue
4
Pages
202-208
ISSN
0166-2236
DOI
10.1016/j.tins.2005.02.001
Cited by
770
References
21
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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