Mitochondria Targeted Therapeutics for Alzheimer’s Disease: The Good. The Bad. The Potential.

Alzheimer’s disease (AD) is the leading cause of dementia. So far, 99.6% of the clinical trials, including those targeting the energy metabolism, have failed to mobilize disease-modifying properties. altered mitochondrial function and disorders of the brain bioenergy systems have long-documented as early events during the development of AD pathology.

The latest progress: While therapeutic approaches that directly promote mitochondrial bioenergetic machine or eliminating reactive oxygen species exhibited limited translatability, emerging strategies targeting non-energetic aspects of mitochondrial provide a new therapeutic target with the potential to modify the risk of AD and development. Growing evidence also reveals an important relationship between mitochondrial phenotype and neuroinflammation via cells.Herein glial metabolic reprogramming, we summarize the main class of mitochondrial-based therapeutic strategies AD. Moreover, the difference in their success when translated from preclinical models to clinical trials aimed. key factors that distinguish the response to the intervention of bioenergy, including sex, APOE genotype and cellular diversity in the brain, which discussed.

We proposes that the future development of AD mitochondrial targeted therapy should consider the interaction between bioenergetics and mechanisms of other diseases that may require specific types of targeting cell- to distinguish between neurons and cells of non-neural. In addition, a successful strategy will likely include stratification by metabolic phenotype that varies by gender and genetic risk profile and dynamic change throughout the course of the disease. As the network expands in intracellular mitochondria integration and systems biology level, intended- votes, either, compared to unintended consequences, bad, will be required to achieve the therapeutic potential of mitochondria.

 Mitochondria Targeted Therapeutics for Alzheimer's Disease: The Good. The Bad. The Potential.
Mitochondria Targeted Therapeutics for Alzheimer’s Disease: The Good. The Bad. The Potential.

Mitochondrial dysfunction in metabolic disorders associated with age.

Aging is a natural biological processes within an organism that is characterized by bioenergetics and downs of life. Mitochondria are important for cellular bioenergetics and thus an important contributor to age-related damage energetics.

In addition, mitochondria play a major role in calcium signaling, redox homeostasis, and thermogenesis makes this organelle major cellular components that dictate the fate of cells. To maintain the quantity and quality, mitochondria undergo several processes such as fission, fusion and mitophagy to remove or replace the faulty mitochondria. While the machine is properly protected bioenergetics, functional decline associated with age and metabolic diseases associated with age is largely the result of a failure in the protective mechanism.

In addition, the byproducts of metabolism such as reactive oxygen species are also helpful in this damaging path. Mitochondrial dysfunction is always considered to be associated with the disease. In addition, studies in recent years have shown that aging contributes to the decay of mitochondrial health by promoting the imbalance in the mitochondrial pathway-arranged keys. Thus, it is important to understand the nexus of mitochondrial dysfunction and age-related diseases. This review focuses on the various aspects of mitochondrial biology and status on the basis of aging and metabolic diseases associated with age. This article is protected by copyright. All rights reserved.

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