Although Alzheimer's is the most common form of dementia, there is still much that scientists do not understand about the disease, but new research offers vital clues to uncovering its origin.
Researchers at Washington University School of Medicine studied genetically modified mice with an Alzheimer's-like disease and found evidence that certain immune cells associated with the disease are actually stimulated by other cells outside the brain.
Researchers believe this discovery could help in finding more effective treatments capable of interrupting this process.
Lead author Hao Hu, a postdoctoral researcher at the University of Washington, said: "This means that we don't just have to look at Alzheimer's inside the brain, but we also have to look outside of it. We need to look at this disease more holistically. This is a disease that affects the brain, but the whole body is actually involved."
The brains of people with Alzheimer's disease become crowded with unfolded forms of two proteins: beta-amyloid and tau. Many researchers have long argued that beta-amyloid, in particular, is the primary driver of brain destruction. But this hypothesis has recently appeared less compelling, or at least more complex than hoped, as the latest anti-amyloid treatments have shown only modest benefits in slowing the disease's progression.
Previous research by the team has pointed to another potential key driver of Alzheimer's symptoms: the accumulation of certain immune cells known as T cells in the brain.
Although the accumulation of amyloid and tau proteins may remain a crucial early aspect of the disease, high levels of T cells, possibly in conjunction with another type of immune cell called microglia, may be the actual trigger for the damage.
In a previous study on mice, researchers removed or blocked the activity of these T cells, which appeared to reduce inflammation and further nerve damage.
T cells are typically activated by another type of immune cell called dendritic cells, and the researchers were particularly interested in a type called the conventional dendritic cell. However, there are relatively few of these dendritic cells in the brain, and those that are present do not appear to be responsible for the T-cell-related damage seen in the Alzheimer's brain, according to the team's previous research. So they decided to look for the potential source elsewhere.
In the new study on mice, researchers genetically modified the brain to remove dendritic cells from extracerebral lymph nodes and other sites. When they did so, it appeared to prevent the accumulation of high levels of T cells in the brain. Furthermore, it seemed to reduce the expected brain damage in the mice while preserving their cognitive function. Remarkably, these improvements occurred even though levels of abnormal tau protein in their brains did not decrease.
These results are limited to mice, so more research will be needed to prove that dendritic cells and T cells are relevant drivers of Alzheimer's in humans.
There are still unanswered questions about this hypothesis, such as what might trigger dendritic cells to send T cells to the brain in the first place. But researchers suspect that the accumulation of abnormal tau protein in the brain is a key trigger.
If this work continues to produce positive results, it may eventually lead to new strategies against Alzheimer's.
The team now plans to test whether removing dendritic cells at an advanced age can still reduce brain damage in mice, a strategy that mimics potential treatments for elderly people at risk of Alzheimer's. They also plan to study the possibility of targeting only specific lymph nodes to get the benefit while minimizing side effects.
The results were published in the journal Nature Neuroscience.
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