Foundation for Mitochondrial Medicine

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Foundation for Mitochondrial Medicine

Alzheimer’s Disease

What is Alzheimer’s disease?

Alzheimer’s disease is a progressive neurodegenerative disorder that causes problems with memory, thinking, and behavior. Symptoms usually develop slowly and progress over time until they become severe enough to interfere with activities of daily living.

There are different types of Alzheimer’s, including variants that are considered familial, often with earlier onset, and those that begin later in life and arise with no family history. Several genetic mutations have been identified in the familial cases. Several causes have been proposed and are currently being researched for the sporadic forms.

Prevalence:

1 in 85 (CDC), an estimated 5.1 million, Americans may have Alzheimer’s disease (National Institute of Aging)

alzheimers-disease-web

What is the role of mitochondrial dysfunction in Alzheimer’s disease?

Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses associated with the etiology and underlying disease components of Alzheimer’s disease.2 Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role in the cause of Alzheimer’s disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to the onset and progression of Alzheimer’s disease.

 

Mitochondrial abnormalities correlate with some of the structural changes that are seen in brains of Alzheimer’s patients. Age-related degradation of mitochondria function is a prime suspect in the pathophysiology of sporadic Alzheimer’s disease.

Emerging Science

Alzheimer’s disease is a progressive neurodegenerative disorder, either assuming a sporadic, age-associated, late-onset form, or a familial form, with early onset, in a smaller fraction of the cases. Whereas in the familial cases several mutations have been identified in genes encoding proteins related with the pathogenesis of the disease, for the sporadic form several causes have been proposed and are currently under debate.

Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of Alzheimer’s disease. Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role as the cause of the disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to its onset and progression.

 


2 Santos RX, Correia SC, Wang X, et al. Alzheimer’s disease: diverse aspects of mitochondrial malfunctioning. Int J Clin Exp Pathol, 2010;3:570-581. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907118/

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