**Conflict of interest**

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

Clinically and pathologically, vessel diseases including atherosclerosis are important diseases in a rapidly aging world. Age-related cerebrovascular dysfunctions result from multiple pathophysiological alterations. The clear one thing is that vascular aging and the aged brain vessels are vulnerable to damages and harmful factors such as the SASPs. Once the cerebral vessels have experienced insults, cognitive decline is eventually followed. The source of insults can be SASP particularly in the aging process. Despite efforts to develop therapeutic targets, it is not possible to identify the processes contributing to the onset of vascular disease and its progression of cognitive decline. Our aging society needed more fundamental approaches for treating aging-related neurodegenerative diseases containing dementia. Preferential treatment might be a preventive chance to neurodegenerative diseases. In the present time when dementia becomes an important issue in public heath, economics, social aspects, as well as the political fields, it should be possible to develop preventing and also therapeutic strategies against progressive dementia with a careful focus on treating vascular health by modulating the SASP.

*Aging, cerebrovascular burden, and developing cognitive decline to vascular dementia. With aging, the number of resident senescent cells displaying SASP increases. The familial genetic backgrounds and vascular risk factors acquired through individual lifestyle or harmful habits, such as smoking, increase vulnerability to vascular damage and neuronal dysfunction. Combined with aging factors, such as SASP, during the aging process, vascular damage and neuronal diseases could lead to susceptibility to cognitive decline, which consequently contributes to the progression of vascular dementia. Abbreviations: SASP, senescence-associated secretory phenotype; APOE4, apolipoprotein E4; PSEN1, presenilin 1; VSMC, vascular smooth muscle cell; EC,* 

This study was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education

**10**

**5. Conclusions**

*endothelial cell.*

**Figure 1.**

**Acknowledgements**

(NRF-2018R1D1A1B07048587).

The authors declare no conflict of interest.
