Genetic engineering of human induced pluripotent stem cells has revealed very specifically how a key mutated protein is involved in familial Alzheimer's. Familial Alzheimer’s is a subset of early-onset Alzheimer's disease that is caused by inherited gene mutations.
Analysis of mitochondrial DNA (mtDNA) in the cerebrospinal fluid has found that both symptomatic Alzheimer’s patients and asymptomatic patients at risk of Alzheimer’s showed a significant decrease in levels of circulating cell-free mtDNA in the CSF. Patients with frontotemporal dementia did not display this.
Analysis of 1,821 Alzheimer’s brains has found that 11% of them actually suffered from a variant called hippocampal sparing Alzheimer’s. This subtype has been neither well recognized nor treated appropriately, but is now revealed to be relatively common.
Genetic analysis of 9,232 older adults (average age 67; range 56-84) has implicated four genes in how fast your hippocampus shrinks with age (rs7294919 at 12q24, rs17178006 at 12q14, rs6741949 at 2q24, rs7852872 at 9p33). The first of these (implicated in cell death) showed a particularly strong link to a reduced hippocampus volume — with average consequence being a hippocampus of the same size as that of a person 4-5 years older.
A review of brain imaging and occupation data from 588 patients diagnosed with frontotemporal dementia has found that among the dementias affecting those 65 years and younger, FTD is as common as Alzheimer's disease. The study also found that the side of the brain first attacked (unlike Alzheimer’s, FTD typically begins with tissue loss in one hemisphere) is influenced by the person’s occupation.