Proteome-wide Mendelian randomization identifies causal plasma proteins in frontotemporal dementia.

What was studied

This study used a gene-based method called Mendelian randomization. It looked for plasma proteins that may cause frontotemporal dementia (FTD) or its subtypes. The abstract says FTD has no disease-modifying treatments. The authors used large datasets of gene variants that affect protein levels.

What they found

Several plasma proteins were linked to FTD. RGS7 and ASAP2 went with higher risk. TMCC3 and VPS29 went with lower risk. Each subtype had its own proteins. S100A13 and TREM1 were seen in the behavioural variant. ING4 and TEX29 were seen in FTD with motor neuron disease. SPINT2 was seen in progressive non-fluent aphasia. UGDH was seen in semantic dementia.

What it means for patients

The authors say the study points to certain plasma proteins in how FTD arises. They say the effects differ by subtype. They say these proteins may serve as markers for sorting patients. They say they may also serve as drug targets.

Why it is not certain yet

The abstract gives no patient numbers. It does not say how large the effects were. It does not say if the findings were tested elsewhere. This kind of study uses gene data, not a trial of a treatment.

Source

Proteome-wide Mendelian randomization identifies causal plasma proteins in frontotemporal dementia.

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