There is evidence, but I agree it is not rigorous and does not rise to the level of proof. I hope it can inspire other researchers to research parts of it more thoroughly.
With respect to Dayan Goodenowe and his Plasmalogen theory, I think the Rush study should be reproduced by other groups. I am no qualified to judge it either, but thinking critically, unless some glaring statistical mistakes were made, or error measuring the levels, or simply that plasmalogen deficiency is a biomarker more than causative (he goes at length as to why he considers it to be the latter), we are talking about natural compounds (Plasmalogen precursors, or IV plasmalogens) that do not require FDA approval, so it should be fairly straightforward to fund, develop and test.
“The clinical implications of this study are obvious. This is the first reported evidence of a metabolic phenotype with the same clinical characteristics as the APOE ε2ε3 genotype. The probability of dementia in participants with either a high PBV or an APOE ε2ε3 genotype was indistinguishable”
“The clinical implications of this study are obvious. This is the first reported evidence of a metabolic phenotype with the same clinical characteristics as the APOE ε2ε3 genotype. The probability of dementia in participants with either a high PBV or an APOE ε2ε3 genotype was indistinguishable”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6523320/