Good news (but dated from Nov. 2019)! Apparently, a woman in Colombia, who died in her 70s, had basically two opposing mutations. One of her mutations should have caused early onset of Alzheimers at around age 40, but she did not develop Alzheimer until her death due to a kind of offsetting, simultaneous mutation that protected her.
"The woman at the center of the study possesses a mutant version of PSEN1, a gene coding for a protein involved in processing amyloid precursor protein (APP) and other peptides. The variant is strongly associated with early-onset Alzheimer’s, with people showing signs of cognitive impairment by their mid-40s, and dementia by the time they’re 50. ... Using brain imaging, researchers found that the woman had extremely high levels of amyloid in her brain by the time she reached 70. However, she had little in the way of other signs of Alzheimer’s pathology, such as neurodegeneration or an accumulation of tau protein.
“It actually illustrates ... for the first time, a very clear dissociation of amyloid accumulation from tau pathology, ... she possessed two copies of a rare mutation in APOE, another gene associated with Alzheimer’s risk. ... using in vitro experiments that the sequence, known in the scientific literature as the Christchurch variant, stops the protein product of the gene from binding strongly to its usual targets—sugar molecules involved in the accumulation of tau and neuron damage—and could thus have had a protective effect. "
APOE Mutation Linked to Protection From Alzheimer's: Case Study | The Scientist Magazine®: A woman whose DNA suggested she'd develop early-onset dementia staved off cognitive decline for decades.
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