**4. Aging and vessel-related cognitive decline**

Dementia is an irreversible cognitive condition. According to a statistical report, 7.7 million people are newly diagnosed with dementia every year [90]. Among these, patients with vascular cognitive impairment and dementia (VCID) compose over 20% of the total dementia patient population [91]. By 2030, the number of older people (>60 years of age) is predicted to increase by 56% compared to the number in 2015, and it will continue to grow year by year. Finally, by 2050, our society will become a superaged society, and it is evident that the prevalence of neurodegenerative diseases will increase. Cognitive-related diseases, such as AD or VaD, will increase by 45% in 2050 compared to 2015 [92].

Mild cognitive impairment (MCI) is included as a cognitive-related disease in the older population. Although MCI is also considered as a pre-step proceeding to dementia, patients with MCI still fortunately have a chance of recovery or at least have a chance to delay the progression of the disease. Therefore, new strategies are urgently needed to diagnose and treat patients with MCI. Some blood factors such as MCP-1 or IL-6 have been suggested to be biomarkers for estimating the progression in cognitive decline because the vascular blood factors are modified in patients with MCI [93]. Some clinical studies have shown that VCID occurs in 25–30% of aged people who have had a previous stroke [94, 95]. Stroke is known to be the second leading cause of cognitive dysfunction. Furthermore, a clinical history of stroke increases the risk of cognitive dysfunction up to fivefold [96, 97]. Therefore, the symptoms of poststroke dementia could be related to the occlusion site, occlusion type, occlusion numbers, and lesion volume in the brain. There are studies that have shown that poststroke cognitive decline is related to the pathology of cerebrovascular disease and dementia, although the mechanisms involved in poststroke dementia are complex [90, 98].

Aging is complex and vulnerable to cognitive decline as well as brain disorders [99]. A recent study concluded that cognitive impairment in aged adults with depression is correlated with the SASP profile [100]. This study showed that the levels of the SASP were highest in participants with both late-life depression (LLD) and MCI (**Figure 1**). This study suggests that cognitive impairment in LLD is linked to an aging-specific molecular profile, which might be an indicator for aging people with LLD who develop dementia [100]. Recent clinical studies have reported that depression and cognitive impairment in aging are associated with the regulation of the SASP: immune-inflammatory response [101], proteostasis [102], signal transduction, and oxidative stress [103].

#### **Figure 1.**

*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, endothelial cell.*

## **5. Conclusions**

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.

#### **Acknowledgements**

This study was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2018R1D1A1B07048587).

**11**

**Author details**

Kyoungjoo Cho

Department of Life Science, Kyonggi University, Suwon, South Korea

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*Address all correspondence to: kcho0611@kgu.ac.kr

provided the original work is properly cited.

*Aging, Cerebrovascular Burden, and Cognitive Decline DOI: http://dx.doi.org/10.5772/intechopen.89854*

The authors declare no conflict of interest.

**Conflict of interest**

*Aging, Cerebrovascular Burden, and Cognitive Decline DOI: http://dx.doi.org/10.5772/intechopen.89854*
