Research Square

Blood protein links to Alzheimer’s differed by genetic risk

Researchers linked 85 blood proteins to Alzheimer’s in people without a key genetic risk variant, compared with 10 in carriers.

Figure 1. Study design and analytical workflow for genetic risk-stratified plasma proteomics of incident AD
Open the figure at full size
Figure 1. Study design and analytical workflow for genetic risk-stratified plasma proteomics of incident ADStudy design and analytical workflow for genetic risk-stratified plasma proteomics of incident ADLeng et al.

Our read

Biomarkers
Studied:
Preprint: cohort study of 18,212 older adults without dementia at enrollment, against APOE ε4 carriers
What changed:
Later Alzheimer’s was linked to 85 blood proteins in APOE ε4 non-carriers, against 10 in carriers
The catch:
Health records could miss Alzheimer’s cases, distorting protein associations
In the record:
The 924th paper on APOE with results in people; 3,703 on record in all. Its result on Alzheimer's disease agrees with 71 of 78 other findings on record; 5 point the other way and 2 found no change.
Why it’s aging research:
It bears on staying healthy in midlife and later life.

Editor of record: Boris Djordjevic · AgingResearch.News

Follow @agingbrief

An observational cohort study followed 18,212 UK Biobank participants aged 60 or older without dementia at enrollment; 52.9% were women. Researchers analyzed 2,911 proteins in blood samples collected at enrollment. Over a mean 12.8 years, 374 participants developed Alzheimer’s disease, identified through health records.

The team grouped participants by whether they carried APOE ε4, a gene variant linked to Alzheimer’s risk, and by a score based on other genetic variants. They identified 85 proteins associated with later Alzheimer’s among non-carriers and 10 among carriers. Across the analyses by genetic risk, the researchers identified 94 proteins newly linked to Alzheimer’s risk.

Why it matters

The authors interpreted the patterns as pointing to protein-related pathways that depend on genetic background in Alzheimer’s disease, an age-related illness.

Caveats

The observational design cannot establish whether the proteins caused Alzheimer’s disease. The preprint has not been peer-reviewed, and the analysis excluded people under 60 and those with dementia at enrollment.

Comments

Be the first to comment.