Alzheimer’s disease is the most common cause of dementia, a group of conditions that affect memory, thinking, and everyday activities.
Millions of people around the world live with Alzheimer’s, and the number is expected to grow as people live longer.
The disease usually develops slowly over many years. At first, people may forget recent conversations or misplace everyday items. As the disease gets worse, they may struggle to recognize loved ones, communicate clearly, or care for themselves.
Although Alzheimer’s has been studied for decades, scientists still do not know exactly what causes it. There is also no cure. Current treatments can help manage some symptoms for a limited time, but they cannot stop or reverse the disease.
Because of this, researchers continue searching for new ways to understand what happens inside the brain during the early stages of Alzheimer’s.
For many years, most Alzheimer’s research has focused on a sticky protein called amyloid-beta. According to the amyloid theory, this protein builds up between brain cells, forming plaques that interfere with communication between nerve cells. Over time, this damage leads to the memory loss and thinking problems seen in people with Alzheimer’s disease.
Another important theory looks at mitochondria. Mitochondria are tiny structures inside almost every cell in the body. They are often called the cell’s power plants because they produce the energy cells need to survive and function.
Brain cells require large amounts of energy to send signals, store memories, and perform other complex tasks. If mitochondria stop working properly, brain cells may become weak or die.
A research team led by Professor Jan Gruber at Yale-NUS College wanted to learn whether problems with energy production might actually begin before amyloid-beta builds up. To investigate this question, they studied tiny worms called Caenorhabditis elegans.
Although these worms are only about one millimeter long, they share many basic biological processes with humans. Scientists have used them for many years to study aging and disease because they grow quickly and are easy to examine.
The researchers discovered that changes in the worms’ mitochondria appeared before large amounts of amyloid-beta accumulated. This finding suggests that problems with the cell’s energy supply may be one of the earliest events in the disease process.
If the same thing happens in people, it could change the way scientists think about Alzheimer’s. Instead of treating amyloid buildup as the first problem, researchers may need to pay more attention to keeping mitochondria healthy.
The team also tested metformin, a medicine that has been safely used for many years to treat type 2 diabetes. After the worms received metformin, their energy production improved. They also lived longer and remained healthier than untreated worms.
These results suggest that restoring normal energy production may help protect cells from the harmful changes linked to Alzheimer’s disease.
The researchers believe this work may also support a broader idea about aging. They suggest that Alzheimer’s and several other diseases linked to growing older may not be completely separate illnesses.
Instead, they may develop because the normal aging process gradually damages cells and reduces their ability to produce energy. If this idea proves correct, treatments that slow the aging process or improve mitochondrial function could help lower the risk of several age-related diseases at the same time.
The scientists caution that these findings are still at an early stage. Results from worms do not always apply to humans because the human brain is much more complex.
More laboratory studies, animal research, and clinical trials will be needed before doctors know whether metformin or other treatments that target mitochondria can help prevent or treat Alzheimer’s disease.
Even so, the study opens an exciting new direction for Alzheimer’s research. Looking beyond amyloid-beta and studying how brain cells make and use energy could lead to new treatments that begin much earlier in the disease process.
The study was led by Professor Jan Gruber and published in the scientific journal eLife. While much more research is needed, the findings provide fresh hope that understanding the role of mitochondria may one day lead to better ways to prevent or slow Alzheimer’s disease.
If you care about Alzheimer’s disease, please read studies that bad lifestyle habits can cause Alzheimer’s disease, and strawberries can be good defence against Alzheimer’s.
For more information about brain health, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
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