One of the strongest findings involved a variant in CCNG1, which was associated with an earlier age of dementia onset. Carriers of the risk allele developed dementia roughly a decade earlier than those without it.

The same variant was also linked to higher levels of TDP-43, a protein implicated in several neurodegenerative diseases, and signs of accelerated brain aging on MRI scans.

The researchers also found that a variant in RHOJ was associated with biological markers of more severe Alzheimer’s disease. Individuals carrying the risk allele had higher levels of total tau and phosphorylated tau 181 in cerebrospinal fluid and a lower Aβ42/Aβ40 ratio—changes commonly associated with Alzheimer’s pathology.