William Mantyh (a former clinical fellow) studied polygenic risk scores of Late Onset Alzheimer's Disease (LOAD), and it's relationship to Early Onset Alzheimer's Disease (EOAD).
The hypothesis was that EOAD might be LOAD with increased polygenic risk scores. To answer that question, Mantyh used a previously validated Polygenic Hazard Score (PHS) in LOAD, and applied it to a cohort of symptomatic EOAD subjects. He found no association between the LOAD PHS, and EOAD's age of onset or disease biomarkers. This findings suggest that EOAD is not a form of LOAD with enriched single nucleotide polymorphisms. Instead, EOAD might be explained by different genetic pathways.
Mounting evidence towards the hetereogenity of AD. Further research is needed.
