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Mitochondrial failures in Alzheimer's disease

Mark A. Smith, PhD

Institute of Pathology, Case Western Reserve University, Cleveland, Ohio.

George Perry, PhD

Gjumrakch Aliev, MD, PhD

Departments of Pathology and the Microscopy Research Center, Case Western Reserve University, Cleveland, Ohio.

Mitochondrial dysfunction and free radical-induced oxidative damage have been implicated in the pathogenesis of several different neurodegenerative diseases such as Parkinson disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and Alzheimer's disease (AD). The defective adenosine triphosphate (ATP) production and increased oxygen radicals may induce mitochondria-dependent cell death because damaged mitochondria are unable to maintain the energy demands of the cell. The role of vascular hypoperfusion-induced mitochondria failure in the pathogenesis of AD now has been widely accepted. However, the exact cellular mechanisms behind vascular lesions and their relation to oxidative stress markers identified by RNA oxidation, lipid peroxidation, or mitochondrial DNA (mt DNA) deletion remain unknown. Future studies comparing the spectrum of mitochondrial damage and the relationship to oxidative stress-induced damage during the aging process or, more importantly, during the maturation of AD pathology are warranted.

Key Words: mitochondria • Alzheimer's disease • hypoperfusion • mitochondrial DNA deletion • amyloid cascade

American Journal of Alzheimer's Disease and Other Dementias®, Vol. 19, No. 6, 345-352 (2004)
DOI: 10.1177/153331750401900611


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