Role of impaired mitochondrial energy metabolism in dementia onset and progression at advanced age

What is it about?

Alzheimer's disease (AD) is historically characterized by three neuropathological signs: amyloid plaques, neurofibrillary tangles, and neuron loss. Recent evidence shows that AD in subjects aged 85 years and older was associated with significantly less amyloid plaque and fibrillary tangle neuropathology than in the young-old population (those aged <85). This paper describes an investigation that we performed using quantitative PCR analyses on brain tissue specimens, validating genome-wide microarray RNA studies previously conducted by our research group.

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Why is it important?

Findings from this study support the hypothesis that the oldest-old AD subjects are characterized by significantly lower AD neuropathology than young-old AD subjects, and that they display brain mitochondrial metabolism impairment. We hypothesize that mitochondrial metabolism impairment may selectively contribute to the development of dementia. Outcomes from this study provide novel insights into the molecular mechanisms underlying clinical dementia in young-old and oldest-old AD subjects, providing novel potential strategies for AD prevention and treatment in oldest-old dementia cases.