For a number of years now, researchers have theorized and found evidence suggesting Alzheimer’s disease may in fact be a type of prion-based disease, capable of being contracted via prion-contaminated meat and transmitted via certain invasive medica…
For a number of years now, researchers have theorized and found evidence suggesting Alzheimer’s disease may in fact be a type of prion-based disease, capable of being contracted via prion-contaminated meat and transmitted via certain invasive medical procedures.
Research published in 2011 found a prion-like protein called TDP-43 in 25% to 50% of Alzheimer’s patients, and research presented in 2014 revealed Alzheimer’s patients with TDP-43 were 10 times more likely to have been cognitively impaired at death than those without it.
More recent research adds further weight to this hypothesis, finding the two hallmark proteins associated with Alzheimer’s — amyloid beta and tau — act as prions, effectively making it a double-prion disease.
Higher levels of prion-like amyloid beta and tau were found in those with early onset of Alzheimer’s who died at an earlier age, with tau buildup showing the strongest correlation.
Compared to a patient who died of Alzheimer’s at the age of 90, a patient who died at 40 had on average 32 times higher amounts of tau prions in their brain.
Other recent studies suggest amyloid beta is an antimicrobial peptide, a primary effector protein of your innate immune system that target bacteria, viruses and fungi, which has led to the development of the antimicrobial protection hypothesis of Alzheimer’s disease. The presence of beta amyloid may not be the actual cause of Alzheimer’s but rather the result of an innate defense mechanism against prion infection.
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