The hypothesis suggests that even a mild infection could result in Alzheimer's. The scenario goes like this: some pathogen (a virus, bacteria or fungi) sneaks into the brain through leaky blood-brain barrier. The immune cells in the brain surround the pathogen and block it by building a protein wall build out of amyloid proteins. The defense is successful -the pathogen dies and disappears - but the amyloid deposits are left behind.
This process has been shown to happen in the lab and in mice and other animals but not in humans. Robert Moir of Harvard noticed that a similar process occurs in the body; the immune system walls immobilizes invaders by building walls around them and then attacks them.
The idea that amyloid was some sort of trash left behind in the brain has gone unchallenged for years. It brings to mind the idea that glial cells were just scaffolding for the neurons or that junk DNA is just junk DNA.
When Moir injected salmonella into the brains of mice that did not produce amyloid, however, they quickly died. Mice able to produce amyloid plaques survived. In fact, the amyloid appeared literally overnight. At the center of each was a bacterium.
There were indications that infections could be triggering Alzheimer's; people with Alzheimer's have a higher incidence of herpesvirus infections.
Another supportive finding is that blood-barrier gets weakest over time at the hippocampus - the seat of memory formation - which is where the plaques in Alzheimer's usually first show up.
The cause of Alzheimer's is probably not the infection, however; it's the inability of some people to clear out the amyloid plaques that form after the infection.
The next step is to use gene sequencing studies to look for microbes in brains of people who had Alzheimer's.
This process has been shown to happen in the lab and in mice and other animals but not in humans. Robert Moir of Harvard noticed that a similar process occurs in the body; the immune system walls immobilizes invaders by building walls around them and then attacks them.
The idea that amyloid was some sort of trash left behind in the brain has gone unchallenged for years. It brings to mind the idea that glial cells were just scaffolding for the neurons or that junk DNA is just junk DNA.
When Moir injected salmonella into the brains of mice that did not produce amyloid, however, they quickly died. Mice able to produce amyloid plaques survived. In fact, the amyloid appeared literally overnight. At the center of each was a bacterium.
There were indications that infections could be triggering Alzheimer's; people with Alzheimer's have a higher incidence of herpesvirus infections.
Another supportive finding is that blood-barrier gets weakest over time at the hippocampus - the seat of memory formation - which is where the plaques in Alzheimer's usually first show up.
The cause of Alzheimer's is probably not the infection, however; it's the inability of some people to clear out the amyloid plaques that form after the infection.
The next step is to use gene sequencing studies to look for microbes in brains of people who had Alzheimer's.
![ME/CFS lecture | Dr Nancy Klimas | 2011 [Chronic Fatigue Syndrome / SEID / New Zealand] - YouTube](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
