As the amyloid cascade hypothesis of Alzheimer’s disease has it, the condition begins with growing levels of amyloid-β in the brain. The amyloid forms solid deposits with a surrounding halo of harmful biochemistry, degrading the function of nearby cells. Perhaps this is caused by failing drainage of cerebrospinal fluid, perhaps by the innate immune response to persistent infections, perhaps by other mechanisms such as the age-related failure of the immune system to clear up molecular waste as aggressively as it should. The amyloid sets the stage for mild cognitive impairment and the later deposition of altered forms of tau protein into neurofibrillary tangles. It is the tau aggregation that is associated with the real damage of Alzheimer’s disease: the inflammation, the major dysfunction, the death of neurons in large numbers.
How exactly is tau wreaking such havoc, however? This is an open question, still awaiting a definitive collection of evidence and consensus. There is the hope that, given a good answer to this question, some form of molecular sabotage could prove to be the basis for a therapy to rescue patients who are far along in