Endocytic Scaffolds At The Crossroads Of Alzheimer’S Disease And Neuronal Aging
Our brain cells, or neurons, are constantly working, and just like the rest of our body, they undergo changes as we age. A recent study sheds light on a crucial cellular process called “endocytosis” and its unexpected role in both normal brain aging and the onset of Alzheimer’s disease.
Think of endocytosis as the cell’s way of “eating” or “drinking.” It’s how cells take in substances from their surroundings by engulfing them in a small pouch made from their outer membrane. This process is vital for many cellular functions, including communication and nutrient uptake.
The research highlights that as neurons get older, they ramp up this endocytosis process specifically for a protein called Amyloid Precursor Protein, or APP. APP is a normal protein found in brain cells. However, when APP is processed in a particular way, it can lead to the creation of sticky fragments known as beta-amyloid. These beta-amyloid fragments are notorious for clumping together to form plaques, a hallmark of Alzheimer’s disease.
The study found that this age-related increase in APP endocytosis directly leads to a greater production of beta-amyloid. This excess beta-amyloid then causes damage to “synapses,” which are the critical junctions where neurons connect and communicate with each other. The loss of these connections is a major factor in the cognitive decline seen in Alzheimer’s.
Essentially, the paper uncovers a mechanism where the natural aging of our brain cells can inadvertently trigger a pathway that contributes to Alzheimer’s pathology. This discovery suggests that targeting the increased endocytosis of APP could be a promising new strategy to prevent or slow down the progression of late-onset Alzheimer’s disease.
Source: link to paper