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Phoenix666 writes:

"Age-related neurodegenerative diseases, like Alzheimer's, progress over a long period of time before they become clinically apparent. The earliest physiological and molecular events are largely unknown," said Mastroeni. "Findings from our laboratory have uncovered early expression changes in nuclear-encoded, but not mitochondrial-encoded mRNAs occurring in one's early 30s, giving us a glimpse into what we suspect are some of the earliest cellular changes in the progression of Alzheimer's disease."

Results of the new study show that specific classes of genes associated with mitochondrial cell respiration display reduced expression levels in patients with Alzheimer's disease, compared with normal patients.

The study also examines gene expression in subjects whose brains show an intermediate level of illness known as mild cognitive impairment. Here, the opposite effect is observed, with relevant genes exhibiting increased levels of expression. The authors suggest this observation may point to some kind of compensatory mechanism in the brain attempting to stave off the disease in its earlier stages.

Further, the study proposes that restoring a specific set of damaged genes linked to mitochondrial function and located in the nuclear DNA of cells may offer a promising strategy for halting the disease's advance.

Journal: Nuclear but not mitochondrial-encoded OXPHOS genes are altered in aging, mild cognitive impairment, and Alzheimer's disease. Alzheimer's and Dementia, 2016; DOI: 10.1016/j.jalz.2016.09.003

Simply put, the mitochondria run out of gas, and Alzheimer's follows.

Original Submission