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Carbonic anhydrase inhibition selectively prevents amyloid β neurovascular mitochondrial toxicity.
Author: DebureLudovic, FossatiSilvia, MadambaStephen M, PavlovEvgeny V, PeixotoPablo M, SolesioMaría E, WisniewskiThomas, de LeonMony J
Original Abstract of the Article :
Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer's disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid β (Aβ)-mediated onset of apoptosis in the mouse bra...See full text at original site
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引用元:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6052473/
データ提供:米国国立医学図書館(NLM)
Carbonic Anhydrase Inhibitors: A New Oasis in the Desert of Alzheimer's Disease
Alzheimer's disease (AD), a devastating neurodegenerative disorder, is like a relentless sandstorm that erodes cognitive function and memory. This research delves into the potential of carbonic anhydrase inhibitors (CAIs) to combat AD by targeting mitochondrial dysfunction, a crucial aspect of the disease's progression.
The researchers explored the effects of methazolamide (MTZ) and acetazolamide (ATZ), two CAIs, on neuronal and vascular cells challenged with amyloid beta (Aβ) – a protein implicated in AD. They discovered that CAIs selectively inhibited Aβ-induced mitochondrial dysfunction without affecting metabolic function, suggesting a targeted approach to protecting mitochondria from the damaging effects of Aβ.
A New Path to Protection
This research offers a promising avenue for treating AD by targeting mitochondrial dysfunction. The CAIs' ability to protect mitochondria from Aβ-induced damage is like finding a hidden oasis in the desert, providing a source of resilience and protection for brain cells. This discovery could lead to the development of new therapeutic strategies for AD, potentially slowing its progression and mitigating its devastating effects.
A Hopeful Horizon for Alzheimer's
This research inspires hope for the future of AD treatment. The potential of CAIs to protect mitochondria from Aβ-induced damage offers a new path to mitigating the devastating effects of this disease. The findings suggest that CAIs, already approved for other medical uses, might be repurposed to combat AD, providing a valuable tool in the fight against this debilitating condition.
Dr. Camel's Conclusion
This research reveals a promising new strategy for combating Alzheimer's disease by targeting mitochondrial dysfunction. Carbonic anhydrase inhibitors (CAIs) show potential to protect mitochondria from the damaging effects of amyloid beta (Aβ), potentially slowing the progression of the disease. This discovery could lead to the development of new and repurposed therapies for AD, offering a glimmer of hope in the desert of this devastating condition.
Date :
- Date Completed 2019-10-07
- Date Revised 2021-01-09
Further Info :
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