No. The beta amyloid protein is the primary 'cause' of Alzheimer's. It builds up in the brain and kills neurons and synapses. Tens of billions of dollars have been spent developing drugs to reduce the amount of amyloid in the brain to try and combat Alzheimer's, none of which has led to an effective treatment.
This newer theory is that the cause of the amyloid build-up is an immune response to the herpes virus increasingly infiltrating the brain (as you get older the blood/brain barrier that protects your brain from infections weakens) so a possible treatment is to try and reduce the levels of herpes infection rather than attacking the amyloid protein which is your body's immune response to the herpes infection.
The APOE4 gene is infamous for increasing amyloid production and being a major risk factor for early-onset Alzheimers and so carriers of the gene are often used in studies to see the effect of treatments. (@subcosmos below has a good explanation of what this gene actually does)
The thing about viral infections of the nervous system is that you don't even need to consider the blood brain barrier. Viruses travel backwards through neurons by hijacking microtubule transport networks, and many groups have hypothesized in the literature that it could be getting into the brain by simply infecting a peripheral nerve and traveling up the spinal chord.
Check out Figure 1 in this paper. The model effectively is that HSV infects a great many people in early life, and becomes latent in neurons until old age. Then it suddenly wakes up again and travels to the brain. All it takes is an infected muscle or other tissue, allowing the virus to get into the nerve.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546524/
Some VERY notable statistics mentioned in the paper : "Such studies have revealed endemic infection rates of 31% in children aged 6–14, rising to 49% in adults aged 14–49, and to a high of 80–90% in the population over 65. In one study of 40 autopsied TGs, HSV-1 sequences were amplified from DNA or RNA extracted from 81% of TGs from demented subjects, and 74% of controls"
I blogged about these connections here, for I think that this retrograde transport phenomenon might explain Tau phosphorylation, which is a secondary hallmark of Alzheimer's and other dementias : https://medium.com/@InfinoMe/cholesterol-have-we-shot-the-me...
As its name implies, the blood brain barrier protects the brain from whatever happens to flow in the blood stream. The herpes virus enters the brain by another channel : the peripheral, somatosensory nerve cells whose axon has a T shape. One prong of the top bar goes to the peripheral tissue, and the other prong goes up to the brainstem.
Expanding further: the blood brain barrier is made of cytoplasmic expansions of astrocytes in the central nervous system. The T-shape sensory cells are part of the peripheral nervous system, their axon ends up in the encephalon.
After reading a bit about it, I think the hypothesis is more that Alzheimer’s is the side effect of the body’s own anti-viral systems acting to contain viruses in the brain.
Most of the latest studies are showing a reduction in Alzheimer’s risk after treating patients who have some form of herpes with anti-viral medication.
Correct, as humans evolved, parasitic infections increased. The APOE gene was a method of slowing down or stopping parastic infection to the brain.
"Among the Tsimane as a whole, adults with APOE4 got poorer scores in these tests. But when the team focused on the people with high parasite levels, they saw that the APOE4 carriers had better mental skills, even outperforming APOE3 carriers who were parasite-free."
No.... APOE is a lipoprotein that transports cholesterol, and viruses jump onto it to get into cells. Amyloid-Beta is what seems to be wrapping around the virus particles to block their transit.
