Power outage in the brain may be source of Alzheimer's
Restoring damaged genes linked to mitochondrial function may offer strategy for halting disease advance
Alzheimer's graphic (stock image).
Credit: © Feng Yu / Fotolia
On Nov. 25, 1901, a 51-year-old woman is admitted to a hospital in Frankfurt, Germany, displaying a bizarre constellation of symptoms. Her behavior is erratic. She shows signs of paranoia as well as auditory hallucinations, disorientation and severe memory impairment. Asked to write her own name, she manages "Mrs.," then lingers over the page, unable to remember the rest. "I have lost myself," she tells the attending physician.
Over time, she will withdraw into her own inscrutable universe, before dying on April 9, 1906.
The tragic case of Auguste Deter might have vanished into the recesses of medical history, but for the following fact: Her doctor, Alois Alzheimer, made a thorough examination of her medical condition, including her excised brain, discovering the telltale amyloid plaques and neurofibrillary tangles characteristic of her illness. Auguste Deter was the first person diagnosed with Alzheimer's disease.
Today, society faces an epidemic of Alzheimer's, with some 5 million afflicted in the U.S. alone. The number is projected to swell to 14 million by midcentury, according to the Centers for Disease Control and Prevention. Of the top 10 leading fatal illnesses, Alzheimer's remains the only one that cannot be prevented, treated or cured.
In new research appearing in the journal Alzheimer's and Dementia, Diego Mastroeni, Paul Coleman and their colleagues at the ASU-Banner Neurodegenerative Disease Research Center (NDRC) and the Biodesign Center for Bioenergetics investigate the role of mitochondria in Alzheimer's disease pathology. Mitochondria act as energy centers for cells and are of central importance in health and disease.
The study builds on earlier work suggesting gene mutations affecting mitochondrial function may be critical in the development -- and pitiless progression -- of the disease.
"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."
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