Groundbreaking study from researchers at The University of Texas Health Science Center at San Antonio uncovers genetic factor that may contribute to the risk of late-onset Alzheimer’s disease, a neurodegenerative condition that currently affects approximately 7 million Americans, a number expected to nearly double by 2050 according to the Alzheimer’s Association. While there is no cure, early detection and treatment can significantly preserve brain function and slow disease progression.

By analyzing more than 230 samples from carriers of risk genes, scientists have uncovered distinct signatures in protein expression in three subtypes of frontotemporal dementia. Their findings help to clarify the underlying biological basis of genetic frontotemporal dementia, and offer a useful resource for future studies and for diagnostic and biomarker development. Frontotemporal dementia is a group of neurodegenerative disorders that arise when the brain’s frontal lobes start to degenerate. Although it’s less common than Alzheimer’s disease, frontotemporal dementia is still a leading cause of dementia worldwide, and it has few approved treatments. Almost a third of cases have a genetic cause, usually due to mutations in genes such as GRN and C9orf72. Here, Aitana Sogorb-Esteve and colleagues leveraged mass spectrometry and proteomics to study proteins in cerebrospinal fluid from a large cohort of people carrying mutations linked to genetic frontotemporal dementia. They examined 238 samples from 71 C9orf72 mutation carriers, 55 GRN mutation carriers, and 36 MAPT mutation carriers – comprising both symptomatic and presymptomatic individuals – as well as from 76 nonsymptomatic, healthy people. The three subtypes of genetic frontotemporal dementia displayed both shared and unique changes in protein patterns. For example, all three types of carriers had shifts in the proteins pentraxin 2 and FABP3, while MAPT carriers alone showed a marked drop in lysosomal proteins. Further analysis identified modules of proteins enriched across the three subtypes, which correlated with more severe disease and cognitive decline. Sogorb-Esteve et al. also found that these proteomic profiles largely overlapped with Alzheimer’s disease, and note that their work could inform research into targeted assays and future diagnostic efforts.

The study, led by the University of Exeter, found that certain bacteria were associated with better memory and attention, while others were linked to an increased risk of Alzheimer’s disease. 

New research from Edith Cowan University (ECU) has shown that diet could influence the risk of both depression and Alzheimer’s disease (AD). Evidence suggests that depressive symptoms are both a risk factor for AD and a reaction to early memory problems.