Alzheimer’s disease is the most common form of dementia in the U.S. – nearly 7 million people have it – and still don’t know exactly what is causing the condition.
“Scientists believe Alzheimer’s disease prevents parts of a cell’s factory from running well,” explained the Alzheimer’s Association. “They are not sure where the trouble starts.”
Researchers in Japan may have just unlocked part of this mystery surrounding Alzheimer’s, according to a pre-print study published in the eLife journal.
“Neuronal aging and neurodegenerative diseases are accompanied by proteostasis [loss of protein homeostasis, a common feature of aging] collapse, while cellular factors that trigger it are not identified,” said the researchers. They used fruit flies to study how mitochondria – parts of cells that provide most of those cells’ chemical energy – might fit into the puzzle of Alzheimer’s.
That puzzle includes plaques and tangles, abnormal structures found in the brains of Alzheimer’s patients. Plaques are deposits of a protein fragment called beta-amyloid and tangles are twisted fibers of another protein called tau. According to the Alzheimer’s Association, they are the “prime suspects in damaging and killing nerve cells.”
Per a press release, researchers from Tokyo Metropolitan University who authored the recent study “identified how proteins collect abnormally in neurons.” They focused on impaired mitochondrial transport in the axon, a portion of nerve cells that carries nerve impulses away from the cell body.
“We found that genetic depletion of axonal mitochondria causes dysregulation of translation and protein degradation,” they said. In particular, they studied eIF2β, a protein subunit. Results of the study indicate that loss of axonal mitochondria can impact proteins related to neurodegenerative diseases such as Alzheimer’s.
However, there’s a catch. According to the eLife journal, the research is “incomplete,” meaning that its claims are only partially supported.
“While these are intriguing observations that are potentially useful, several technical weaknesses limit the interpretation and mean the evidence supporting the current claims is incomplete,” said an eLife assessment.
It is known that microscopic changes happen in the brain’s 100 billion nerve cells before Alzheimer’s symptoms begin.
“There is now clear evidence that the development and progressive accumulation of [amyloid beta] pathology occurs years before dementia symptoms begin, thereby providing a window of opportunity for intervention prior to symptom onset,” said the description of a 2022 study from researchers at Washington University School of Medicine in St. Louis.
Scientists have also linked other factors to the development of the disease, including genes, head injury and damage to the heart and blood vessels, per the Alzheimer’s Association. While there is not yet a cure for Alzheimer’s there has been a treatment approved to slow the progression of the disease (another treatment option was discontinued this year). Additionally, research from this year signals that a blood test may soon be available to diagnose Alzheimer’s