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Molecular Targets in Alzheimer's Disease
Geir Bjørklund1, Jan Aaseth2,3, Maryam Dadar4
1Council for Nutritional and Environmental Medicine, Toften 24, 8610, Mo i Rana, Norway. bjorklund@conem.org.
Molecular Neurobiology
|April 11, 2019
Summary
Alzheimer's disease involves amyloid beta and tau proteins. This review explores molecular links like oxidative stress and mitochondrial dysfunction, revealing potential therapeutic targets for this neurodegenerative disorder.
Area of Science:
- Neurodegenerative Disorders
- Molecular Biology
- Gerontology
Background:
- Alzheimer's disease (AD) is a prevalent neurodegenerative disorder in aging populations.
- AD pathogenesis is characterized by amyloid beta (Aβ) plaques and tau tangles.
- These pathological hallmarks are increasingly understood to be interconnected.
Purpose of the Study:
- To review molecular mechanisms linking Aβ and tau toxicities in Alzheimer's disease.
- To elucidate the roles of oxidative stress, aging, and mitochondrial dysfunction in AD.
- To identify potential molecular targets for AD treatment.
Main Methods:
- Literature review of molecular mechanisms in AD pathogenesis.
- Analysis of experimental data on Aβ and tau interactions.
- Synthesis of information on oxidative stress, aging, and mitochondrial roles.
Main Results:
- Identified key molecular pathways linking Aβ and tau pathologies.
- Highlighted the contribution of oxidative stress, aging, and mitochondrial dysfunction.
- Emphasized the interplay between these factors in AD development.
Conclusions:
- Understanding the molecular interplay between Aβ and tau is crucial for AD treatment.
- Targeting common pathophysiological pathways may offer therapeutic strategies.
- Further research into these mechanisms could lead to novel treatments for Alzheimer's disease.