(Open access funding provided by Semmelweis University)
(TKP2021-NKTA-47)
Nemzeti Kardiovaszkuláris Laboratórium(RRF-2.3.1-21-2022-00003) Támogató: NKFIH
(TKCS-2021/32)
(EKÖP-2024–2) Támogató: New National Excellence Program
Szakterületek:
Geriátria és gerontológia
Vascular cognitive impairment (VCI) is a leading cause of age-related cognitive decline,
driven by cerebrovascular dysfunction and cerebral small vessel disease (CSVD). Emerging
evidence suggests that cerebromicrovascular endothelial senescence plays an important
role in the pathogenesis of VCI by promoting cerebral blood flow dysregulation, neurovascular
uncoupling, blood–brain barrier (BBB) disruption, and the development of cerebral
microhemorrhages (CMHs). This review explores the concept of cerebromicrovascular
senescence as a continuum of vascular aging, linking macrovascular atherosclerosis
with microvascular dysfunction. It examines the mechanisms by which endothelial senescence
drives neurovascular pathology and highlights the impact of cardiovascular risk factors
in accelerating these processes. We examine preclinical and clinical studies that
provide compelling evidence that atherosclerosis-induced microvascular senescence
exacerbates cognitive impairment. In particular, findings suggest that targeting senescent
endothelial cells through senolytic therapy can restore cerebrovascular function and
improve cognitive outcomes in experimental models of atherosclerosis. Given the growing
recognition of microvascular senescence as a therapeutic target, further research
is warranted to explore novel interventions such as senolytics, anti-inflammatory
agents, and metabolic modulators. The development of circulating biomarkers of vascular
senescence (e.g., senescence-associated secretory phenotype [SASP] components and
endothelial-derived extracellular vesicles) could enable early detection and risk
stratification in individuals at high risk for VCI. Additionally, lifestyle modifications,
including the Mediterranean diet, hold promise for delaying endothelial senescence
and mitigating cognitive decline. In conclusion, cerebromicrovascular senescence is
a key mechanistic link between atherosclerosis and cognitive impairment. Addressing
microvascular aging as a modifiable risk factor through targeted interventions offers
a promising strategy for reducing the burden of VCI and preserving cognitive function
in aging populations.