Cerebral Small Vessel Disease as a Contributor to Neurodegenerative Disorders

Cerebral small vessel disease (CSVD) comprises a spectrum of pathological processes that injure arterioles, capillaries and venules within the brain. Traditionally recognised as a vascular cause of lacunar stroke and vascular cognitive impairment, CSVD is now appreciated as a pervasive, age‑related substrate that converges with canonical proteinopathies to shape the clinical course of many neurodegenerative disorders. Emerging imaging, fluid biomarker and neuropathological data demonstrate that white‑matter hyperintensities, microinfarcts, microbleeds, enlarged perivascular spaces and microvascular blood‑brain‑barrier (BBB) failure accelerate amyloid‑β deposition, tau propagation, α‑synuclein aggregation and neuroinflammation. CSVD thereby lowers brain resilience, hastens cognitive and motor decline, and complicates therapeutic response in Alzheimer’s disease (AD), Parkinson’s disease (PD), dementia with Lewy bodies (DLB), frontotemporal degeneration (FTD) and mixed dementias. This narrative review (≈3000 words) summarises epidemiology, mechanistic links, imaging and fluid correlates, disease‑specific evidence, and therapeutic prospects, contending that CSVD represents a tractable target for delaying or preventing neurodegeneration.

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Publication Details

Journal
Neurology Letters
Published
2025-05-08
DOI
https://doi.org/10.61882/nl.4.1.64
Primary Topic
Canadian Policy and Governance
Type
article
Field-Weighted Citation Impact
0.00
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article

Cerebral Small Vessel Disease as a Contributor to Neurodegenerative Disorders

Neurology Letters
Canadian Policy and Governance
article

Cerebral Small Vessel Disease as a Contributor to Neurodegenerative Disorders

article en

Abstract

Cerebral small vessel disease (CSVD) comprises a spectrum of pathological processes that injure arterioles, capillaries and venules within the brain. Traditionally recognised as a vascular cause of lacunar stroke and vascular cognitive impairment, CSVD is now appreciated as a pervasive, age‑related substrate that converges with canonical proteinopathies to shape the clinical course of many neurodegenerative disorders. Emerging imaging, fluid biomarker and neuropathological data demonstrate that white‑matter hyperintensities, microinfarcts, microbleeds, enlarged perivascular spaces and microvascular blood‑brain‑barrier (BBB) failure accelerate amyloid‑β deposition, tau propagation, α‑synuclein aggregation and neuroinflammation. CSVD thereby lowers brain resilience, hastens cognitive and motor decline, and complicates therapeutic response in Alzheimer’s disease (AD), Parkinson’s disease (PD), dementia with Lewy bodies (DLB), frontotemporal degeneration (FTD) and mixed dementias. This narrative review (≈3000 words) summarises epidemiology, mechanistic links, imaging and fluid correlates, disease‑specific evidence, and therapeutic prospects, contending that CSVD represents a tractable target for delaying or preventing neurodegeneration.

Neurology LettersVol. 4(1)
Fortis Healthcare (IN), Fortis Hospital (IN), Govind Ballabh Pant Hospital (IN)
Openalex Percentile: Top 40%
Canadian Policy and Governance
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