Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease.
Arteriolosclerosis
Blood–brain barriers (BBB)
Cerebral amyloid angiopathy (CAA)
Cerebral small vessel disease (cSVD)
Glymphatic drainage
Hypoperfusion/Hypoxia
Intramural periarterial drainage (IPAD)
Vascular cognitive impairment and dementia (VCID)
Vascular inflammation
Journal
Molecular neurodegeneration
ISSN: 1750-1326
Titre abrégé: Mol Neurodegener
Pays: England
ID NLM: 101266600
Informations de publication
Date de publication:
11 07 2023
11 07 2023
Historique:
received:
02
02
2023
accepted:
28
06
2023
medline:
13
7
2023
pubmed:
12
7
2023
entrez:
11
7
2023
Statut:
epublish
Résumé
Vascular cognitive impairment and dementia (VCID) is commonly caused by vascular injuries in cerebral large and small vessels and is a key driver of age-related cognitive decline. Severe VCID includes post-stroke dementia, subcortical ischemic vascular dementia, multi-infarct dementia, and mixed dementia. While VCID is acknowledged as the second most common form of dementia after Alzheimer's disease (AD) accounting for 20% of dementia cases, VCID and AD frequently coexist. In VCID, cerebral small vessel disease (cSVD) often affects arterioles, capillaries, and venules, where arteriolosclerosis and cerebral amyloid angiopathy (CAA) are major pathologies. White matter hyperintensities, recent small subcortical infarcts, lacunes of presumed vascular origin, enlarged perivascular space, microbleeds, and brain atrophy are neuroimaging hallmarks of cSVD. The current primary approach to cSVD treatment is to control vascular risk factors such as hypertension, dyslipidemia, diabetes, and smoking. However, causal therapeutic strategies have not been established partly due to the heterogeneous pathogenesis of cSVD. In this review, we summarize the pathophysiology of cSVD and discuss the probable etiological pathways by focusing on hypoperfusion/hypoxia, blood-brain barriers (BBB) dysregulation, brain fluid drainage disturbances, and vascular inflammation to define potential diagnostic and therapeutic targets for cSVD.
Identifiants
pubmed: 37434208
doi: 10.1186/s13024-023-00640-5
pii: 10.1186/s13024-023-00640-5
pmc: PMC10334598
doi:
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
46Subventions
Organisme : NIA NIH HHS
ID : RF1 AG057181
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG068034
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG071226
Pays : United States
Organisme : NIA NIH HHS
ID : U19 AG069701
Pays : United States
Informations de copyright
© 2023. The Author(s).
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