Mitochondria as a target for neuroprotection: implications for Alzheimer´s disease

Abstract

Alzheimer's disease (AD), the most common form of dementia, is marked by progressive loss of memory and impairment of cognitive ability. Despite decades of intensive research and scientific advances, the intricate pathogenic mechanisms of AD are still not fully understood and, consequently, an effective treatment is yet to be developed. As widely accepted, the alterations of mitochondrial function are actively engaged in a plethora of neurodegenerative diseases, including AD. With growing interest in the mitochondria as a potential target for understanding AD, it has even been hypothesized that deficits in these organelles may be at the heart of the progression of AD itself. Areas covered: The purpose of this review is to summarize relevant studies that suggest a role for mitochondrial (dys)function in AD and to provide a survey on latest developments regarding AD-related mitochondrial therapeutics. Expert commentary: As outlined in a plethora of studies, there is no doubt that mitochondria play a major role in several stages of AD progression. Even though more in-depth studies are needed before pharmaceutical industry can apply such knowledge to human medicine, the continuous advances in AD research field will certainly facilitate and accelerate the development of more effective preventive or therapeutic strategies to fight this devastating disease.

Keywords: Alzheimer´s disease; axonal transport; bioenergetics and oxidative stress; dynamics and quality control; mitochondrial function; mitochondrial-directed therapeutics.