I belong to a group of neuroscientists who concentrate their studies on neurodegenerative diseases such as Alzheimer’s dementia, Parkinson’s disease, and ALS.
The group releases summaries of the latest research in the field of neurodegeneration, along with comments by member neuroscientists.
One of our latest releases was a discussion of some research from Spain that found evidence of mold throughout the brain of 100 percent of Alzheimer’s patients examined — and none in the brains of healthy control subjects.
The idea that fungal infections might be related to dementia is not new. In 1910, Oskar Fischer, a contemporary of Alois Alzheimer, suggested that fungi were a possible cause of dementia.
Since then, a number of other infectious agents have been suspected, including chlamydia and herpes simplex-1.
In a previous study, these same researchers found fungi in Alzheimer’s brains but not normal control brains.
These researchers used special antibodies to identify the fungi and show that they were fully intact organisms.
The fungi were concentrated in the same areas of the brain as we see the greatest pathology in Alzheimer’s dementia: the entorhinal cortex, hippocampus, frontal cortex, and cerebellum.
In all, the researchers found six different species of fungi — all of which are commonly found on skin and in soil.
Interestingly, there is a mechanism by which these mold fungi could indeed trigger and then drive brain degeneration.
It is known that when the brain is infected it becomes highly sensitive to systemic inflammation (immune stimulation) — that is, immune stimulation elsewhere in the body.
The body’s immune system alerts the brain’s own immune system — cells called microglia — and that produces prolonged inflammation and immunoexcitotoxicity in the brain.
The mold primes these microglia so that they react much more intensely than they normally would, thus pouring out massive amounts of inflammatory chemicals and excitotoxins — exactly the process we see in Alzheimer’s disease.
But not all are convinced that these findings are fully valid.
One criticism was that the immunolabeling used in the study is nonspecific and could be labeling a polysaccharide commonly found in Alzheimer’s brains.
The only problem with this criticism is that the researchers also demonstrated that there was fungal DNA, which makes it more likely it was indeed living fungus.
The main criticism, however, was about the timing of the fungal infection.
Is the mold merely an opportunist, infecting the brain long after the disease has smoldered, not actually participating in the pathology?
To determine whether or not that is the case, future studies will have to examine brains for infection early in the course of the disease.
However, there is one noteworthy case in which a person was infected with a brain cryptococcal fungi and developed dementia. After being successfully treated, the dementia subsided.
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