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

ABSTRACT

Introduction: 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
• mitochondrial function
• bioenergetics and oxidative stress
• dynamics and quality control
• axonal transport
• mitochondrial-directed therapeutics

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

The authors’ work is supported by FEDER funds through the Operational Programme Competitiveness Factors - COMPETE and national funds by FCT - Foundation for Science and Technology under the project (PEstC/SAU/LA0001/2013-2014) and strategic project UID/N/NEU/04539/2013. S Cardoso is recipient of a PostDoc fellowship from the Fundação para a Ciência e a Tecnologia (FCT) (SFRH/BPD/95770/2013).