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Gene variant protecting against Alzheimer’s decreases plasma beta-amyloid levels

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The METSIM data comprises 10,000 men living in the eastern part of Finland and the findings were published in Annals of Neurology

A recent research from the University of Eastern Finland shows that the APP gene variant protecting against Alzheimer’s disease significantly decreases plasma beta-amyloid levels in a population cohort.

According to the study, a 30 per cent life-long decrease in beta-amyloid levels is not associated with detrimental effects on lipid or glucose metabolism, or on any other metabolic factors.

The findings, drawing on the data of the METSIM (METabolic Syndrome In Men) study ongoing at the University of Eastern Finland, were published in Annals of Neurology.

Research groups focusing on Alzheimer’s disease and diabetes at the University of Eastern Finland now show that the APP A673T gene variant, which is a variant in the amyloid precursor protein gene protecting against Alzheimer’s disease, leads to an average of 30 per cent decreased levels of the beta-amyloid subtypes 40 and 42. The effects of this previously discovered gene variant were analysed by utilising data from the METSIM study. The METSIM data comprises 10,000 men living in the eastern part of Finland.

Reportedly, Approximately 0.3 per cent of the population are carriers of the APP A673T gene variant. Although the variant itself is rare, the observed association with decreased plasma beta – amyloid levels is important from the viewpoint of Alzheimer’s drug trials. Several on-going drug trials for Alzheimer’s disease focus on decreasing beta-amyloid levels in the brain tissue. The findings from the population cohort in eastern Finland show that a life-long decrease in beta-amyloid levels is not associated with detrimental effects on lipid or glucose metabolism, or on any other metabolically relevant events.

Furthermore, the findings also provide support for the amyloid cascade hypothesis, a hypothesis which is key in Alzheimer’s research and which has recently been heavily questioned due to failed beta-amyloid based drug trials and treatment experiments. According to the hypothesis, the accumulation of beta-amyloid in the brain plays a key role in Alzheimer’s disease.

The findings on the role of the APP A673T gene variant in Alzheimer’s disease facilitate the planning of future research. This insight, in turn, will enable the identification of new drug targets, increasingly good predictive biomarkers and the development of personalised medical applications.

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