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Review
. 2024;20(3):63-76.
doi: 10.2174/011573403X278550240221112636.

Cross Talks between CNS and CVS Diseases: An Alliance to Annihilate

Affiliations
Review

Cross Talks between CNS and CVS Diseases: An Alliance to Annihilate

Shivani Chib et al. Curr Cardiol Rev. 2024.

Abstract

Cardiovascular and neurological diseases cause substantial morbidity and mortality globally. Moreover, cardiovascular diseases are the leading cause of death globally. About 17.9 million people are affected by cardiovascular diseases and 6.8 million people die every year due to neurological diseases. The common neurologic manifestations of cardiovascular illness include stroke syndrome which is responsible for unconsciousness and several other morbidities significantly diminished the quality of life of patients. Therefore, it is prudent need to explore the mechanistic and molecular connection between cardiovascular disorders and neurological disorders. The present review emphasizes the association between cardiovascular and neurological diseases specifically Parkinson's disease, Alzheimer's disease, and Huntington's disease.

Keywords: Alzheimer’s disease; Cardiovascular disorders; Huntington’s disease; Parkinson’s disease; neurological disorders; oxidative stress..

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Conflict of interest statement

The authors declare no conflict of interest, financial or otherwise.

Figures

Fig. (1)
Fig. (1)
Common pathways and risk factors of CDs and PD. Abbreviations: ROS- Reactive oxygen species, ox-LDL-oxidized low-density lipoproteins.
Fig. (2)
Fig. (2)
Cardiovascular and Neurotoxic Effects of Aβ in Brain parenchymal and cardiac. Brain Αβ deposits initiate many biological steps that associated in neurons dysfunctioning and manifested as diminish cognitive ability and potentiate Alzheimer. The depositions in cardiac are accompanying with cardiomyocyte dysfunction. Increase vascular stiffening, vascular inflammation and atherosclerosis. Cardiac dysfunctioning leads to cerebral hypoperfusion, Alzheimer, or dementia.
Fig. (3)
Fig. (3)
Brain-heart pathogenesis in Huntington’s disease.

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