Abnormalities in the brain’s cellular power plants, known as mitochondria, may drive early Alzheimer’s processes — even before the telltale amyloid plaque that marks the disease starts forming in the brain.
The finding suggests that treatments that target the abnormal energy-making processes may be a new way of approaching Alzheimer’s treatment.
The study, “Nuclear but not mitochondrial-encoded OXPHOS genes are altered in aging, mild cognitive impairment, and Alzheimer’s disease,” was published in the journal Alzheimer’s and Dementia.
Mitochondria are crucial to health because they are the only cellular structures that convert nutrients to energy. The process, called oxidative phosphorylation, involves a number of protein complexes that are built from two sets of genes.
One set is in the cell nucleus. The other is in the mitochondria, which has its own genome. There is a general consensus that mitochondrial processes become less efficient with age. But it isn’t clear if specific changes can herald the development of Alzheimer’s.
Researchers from the Arizona State University’s Banner Neurodegenerative Disease Research Center and the Biodesign Center for Bioenergetics analyzed the brains of deceased people to try to better understand the genes that give rise to energy-making complexes.
The team focused on the hippocampus, a brain region crucial for memory processing. To get an idea of how aging and disease affect the genes, the team looked at 44 brains of people with normal brain function aged 29 to 99, 10 brains of people with mild cognitive impairment, and 18 with Alzheimer’s disease.
The mitochondria genes functioned about the same from group to group. But the nuclear genes controlling mitochondrial processes were less active in older people with normal cognitive function and in Alzheimer’s patients.
The researchers might have concluded that the drop in nuclear gene activity was solely related to aging if not for another finding: Gene activity actually increased in those with mild cognitive impairment, the first stage of dementia.
Researchers suspect the increase was a response to as yet unidentified early disease processes.
“Although plaques and tangles remain as the definitive neuropathological hallmark of the disease, plaques do not correlate at all with degree of cognitive impairment in Alzheimer’s disease and tangles correlate only slightly,” Paul Coleman, senior study investigator, said in a news release.
“We further know that plaques and tangles are latecomers in the cascade of events that cause the dementia” of Alzheimer’s, Coleman said. The implication was that the findings may serve as an early disease marker that correlates more closely with the degree of disease than current analyses of plaques and tangles.
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