Alzheimer’s disease is the most common brain disorder affecting older adults around the world. It is also the leading cause of dementia, a condition that slowly damages memory, thinking ability, and everyday functioning.
As people live longer, Alzheimer’s has become an increasing public health concern. Millions of families are affected by the disease, and the number of cases is expected to rise in the coming decades.
Despite many years of research, scientists still do not fully understand what causes Alzheimer’s disease. There is also currently no treatment that can stop or cure it. Most available medications can only help manage symptoms for a limited time. Because of this, researchers around the world continue to search for the underlying causes of the disease.
For many years, the most widely accepted explanation has been the “amyloid hypothesis.” According to this theory, Alzheimer’s begins when a protein called amyloid-beta starts to accumulate in the brain.
These proteins stick together and form sticky clumps known as plaques. Scientists believe these plaques can damage brain cells and disrupt communication between neurons, eventually leading to memory loss and other symptoms of dementia.
However, many scientists have begun to question whether amyloid plaques are the real starting point of the disease. Some researchers believe the plaques might be a later consequence rather than the original cause. This has led to the development of another idea known as the mitochondrial or metabolic theory of Alzheimer’s disease.
Mitochondria are tiny structures inside cells that act like power stations. Their main job is to produce the energy that cells need to survive and function.
Brain cells require large amounts of energy because they must constantly send signals and maintain complex connections. If mitochondria stop working properly, brain cells may not receive the energy they need to stay healthy.
A recent study by scientists at Yale‑NUS College has provided new evidence supporting this metabolic explanation. The research suggests that problems with cell metabolism and energy production may happen much earlier than the buildup of amyloid plaques.
The study was led by researcher Jan Gruber and published in the scientific journal eLife. The team wanted to understand whether energy problems inside cells could appear before the well-known protein buildup linked to Alzheimer’s.
To explore this question, the researchers used a tiny worm called Caenorhabditis elegans. Although these worms are extremely small, they are commonly used in scientific research because many of their cellular processes are similar to those found in human cells. This makes them a useful model for studying aging and disease.
When the scientists observed these worms, they noticed something important. The worms showed clear signs of metabolic problems very early, long before any buildup of amyloid-like proteins could be detected. In other words, the cells began to struggle with energy production first, and the protein accumulation came later.
This finding suggests that the breakdown of normal cell metabolism might trigger the chain of events that eventually leads to Alzheimer’s disease.
The researchers then tested whether improving metabolism could help reverse these problems. To do this, they used metformin, a widely used medication that doctors often prescribe to treat type 2 diabetes. Metformin helps regulate how the body processes energy and sugar.
When the worms were treated with metformin, the scientists observed remarkable improvements. The drug appeared to correct the metabolic problems in the worms’ cells. As a result, the worms became healthier and even lived longer than untreated worms.
These findings suggest that restoring normal metabolism may help protect cells from the damage that leads to neurodegenerative diseases like Alzheimer’s.
The researchers believe this discovery could change how scientists think about Alzheimer’s and other diseases linked to aging. Instead of focusing only on the buildup of harmful proteins after symptoms appear, researchers might need to pay more attention to the earlier changes that occur in the body’s metabolism.
Problems with mitochondria and energy production are common features of aging. As people grow older, the efficiency of mitochondria often declines. This decline may increase the risk of many diseases, including Alzheimer’s, Parkinson’s disease, and other conditions related to aging.
Because of this, the study suggests that protecting mitochondrial function and maintaining healthy metabolism could become an important strategy for preventing these diseases.
Another key message from the research is the importance of early action. By the time memory loss appears in Alzheimer’s disease, damage in the brain has often been developing for many years. If metabolic problems occur even earlier, treatments that target these issues might help prevent the disease before serious brain damage occurs.
The findings from Yale‑NUS College do not yet prove that metabolism is the sole cause of Alzheimer’s, but they provide strong evidence that energy problems inside cells may play a crucial role.
Scientists hope that future studies will explore whether similar metabolic defects occur in humans and whether medications like metformin could help protect brain health.
The research led by Jan Gruber and published in eLife offers an important new perspective on Alzheimer’s disease. By focusing on how cells generate energy, scientists may eventually develop new ways to slow aging processes, protect brain cells, and reduce the risk of dementia.
If these ideas prove correct, improving mitochondrial health could become a key part of preventing not only Alzheimer’s disease but many other conditions that develop as people grow older.
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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