Are Alzheimer's (and other Neuroimmune Diseases) Caused by Infection?

Cort

Founder of Health Rising and Phoenix Rising
Staff member
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.
 

h3ro

Active Member
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.
Seems that the cause is whatever caused the leaky blood-brain barrier then, rather than the infection that has snuck in afterwards.
 

Who Me?

Well-Known Member
Dr Younger had a hypothesis about what causes the blood brain barrier to leak. I can't remember exactly what he said but he talks about it in the video posted last week.
 

Remy

Administrator
Beta amyloid is apparently an antibiotic...getting rid of it (the focus of most AD research in the past) might have really made things worse.

A new study from Massachusetts General Hospital (MGH) investigators provides additional evidence that amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection. Their study published in Science Translational Medicine finds that expression of human amyloid-beta (A-beta) was protective against potentially lethal infections in mice, in roundworms and in cultured human brain cells. The findings may lead to potential new therapeutic strategies and suggest limitations to therapies designed to eliminate amyloid plaques from patient's brains.

"Neurodegeneration in Alzheimer's disease has been thought to be caused by the abnormal behavior of A-beta molecules, which are known to gather into tough fibril-like structures called amyloid plaques within patients' brains," says Robert Moir, MD, of the Genetics and Aging Research Unit in the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND), co-corresponding author of the paper. "This widely held view has guided therapeutic strategies and drug development for more than 30 years, but our findings suggest that this view is incomplete."
Full text here.
 

loki

Well-Known Member
ye
Beta amyloid is apparently an antibiotic...getting rid of it (the focus of most AD research in the past) might have really made things worse.



Full text here.
yeah, right! A-beta is an antibiotic. it also seems to be necessary for the transportation of information. there are some risk factors for alzheimer's, like high cholesterol, mutations of APP gene, mutations of ApoE gene... and in the end, what drives the neurodegeneration is the immune system trying to clear A-Beta, yet unsuccessfully, which leads to collateral nerve damage.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Seems that the cause is whatever caused the leaky blood-brain barrier then, rather than the infection that has snuck in afterwards.
Good point! There are two key parts; one - the virus is able to get access to the brain and two - people who are unable to clear the amyloid deposits that encase the virus get Alzheimer's. I imagine that Alzheimer's is largely a disease of the elderly because the BBB gets more ragged over time.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member

Cort

Founder of Health Rising and Phoenix Rising
Staff member
ye

yeah, right! A-beta is an antibiotic. it also seems to be necessary for the transportation of information. there are some risk factors for alzheimer's, like high cholesterol, mutations of APP gene, mutations of ApoE gene... and in the end, what drives the neurodegeneration is the immune system trying to clear A-Beta, yet unsuccessfully, which leads to collateral nerve damage.
So the amyloid deposits are not necessarily the issue - its an immune problem..
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Then what explains early onset?
The fact that Alzheimer's mostly shows up in older people doesn't mean that younger people might not have problems with the blood brain barrier - probably for other reasons. Older people just have more problems with it in general.
 

loki

Well-Known Member
So the amyloid deposits are not necessarily the issue - its an immune problem..
that's right, it's like in every neurodegenerative disease (MS, PD, HD..) that the main part of the destruction is driven by the immune system. So, in Alzheimer's it's a good approach to target TNF-a and other cytokines, that improves the symptoms and attenuates neurodegeneration. There are some impressive videos on TNF-a inhibitors like Enbrel that were administered to AD patients (perispinal), they began to 'come back' to the world!
That clearly highlights the autoimmune pathology in AD.
 

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