With the discovery of Carbonic Anhydrase (CA) and its isoenzymes in
various Alzheimer’s 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 didn’t 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 Alzheimer’s 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.
Keywords: Alzheimer’s disease, ATZ, Biomarker, CAII, Carbonic anhydrase, Carbonic anhydrase inhibitors, MTZ, Oxidative stress, ROS.
