Effects of Carbonic Anhydrase Inhibitors on Mitochondrial Dysfunction and Consequently on Alzheimers Disease

- Authors: Devyani Bhatnagar1, Shreya Ladhe2, Dileep Kumar3
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View Affiliations Hide Affiliations1 Department of Pharmaceutical Chemistry, Poona College of Pharmacy, Bharati Vidyapeeth (Deemed to be University), Erandwane, Pune 411038, Maharashtra India 2 Department of Pharmaceutical Chemistry, Poona College of Pharmacy, Bharati Vidyapeeth (Deemed to be University), Erandwane, Pune 411038, Maharashtra India 3 Department of Pharmaceutical Chemistry, Poona College of Pharmacy, Bharati Vidyapeeth (Deemed to be University), Erandwane, Pune 411038, Maharashtra India
- Source: Enzymatic Targets for Drug Discovery Against Alzheimer's Disease , pp 205-220
- Publication Date: December 2023
- Language: English


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With the discovery of Carbonic Anhydrase (CA) and its isoenzymes in various Alzheimers disease (AD) models and the brain of AD patients, the role of CA in AD pathology has become of keen interest among scholars around the world. Several experiments were performed to investigate the same, albeit they didnt provide us with the exact mechanism through which CAs are involved in AD progression, but they gave us an important insight into the beneficial outcomes of CA inhibition. Carbonic Anhydrase Inhibitor (CAI) administration showed a significant reduction in the release of the proapoptotic factor- Cytochrome C (cyt C) from the challenged mitochondria (under oxidative stress). Thus, a link between ageing, oxidative stress, mitochondria dysfunction and pathogenesis of Alzheimers disease was established. Treatment with CAI indirectly lowers neuronal loss and, thus, cognitive impairment, which are characteristic features of AD. Though, the precise functions of CA in exaggerating or mediating AD still remain hazy, with the support of various scholarships globally, the use of CAII (an isoenzyme of CA) as a potential biomarker for AD can be proposed.<br>
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