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A 3D visualization of lectin-stained blood vessels (magenta) and Thioflavin-Sa€“positive (yellow) amyloid plaques in the brain of a mouse model of Alzheimera€™s disease. A pathological hallmark of AD is the accumulation of protein fragments between nerve cells in the brain.
These studies provide a significant preclinical validation for GPR3 and set the bar for therapeutic validation in the development of AD drug targets.
Scientists from VIB and KU Leuven have discovered a new target molecule for the development of a treatment against Alzheimer's disease.
Alzheimer's disease (AD) is the most common form of dementia and is characterized by the formation of I?-amyloid plaques throughout the brain.
Tackling brain inflammation ameliorates Alzheimer's disease (AD), according to a study published in The Journal of Experimental Medicine. For decades, scientists have known that people with two copies of a gene called apolipoprotein E4 (ApoE4) are much more likely to have Alzheimer's disease at age 65 than the rest of the population.

A research project has shown that an experimental model of Alzheimer's disease can be successfully treated with a commonly used anti-inflammatory drug.
Iowa State University researchers have identified a protein essential for building memories that appears to predict the progression of memory loss and brain atrophy in Alzheimer's patients. With more than 7.5 million new cases of Alzheimer's disease a year, the race to find a vaccine and effective treatment for dementia is growing by the day. These abnormal clusters of protein fragments build up between nerve cells and disrupt communication in the brain, which makes them prime suspects for causing Alzheimer's Disease (AD). It is characterised by a gradual degeneration of the brain networks that are involved in memory and cognition. These protein fragments are created by secretases, enzymes that cleave proteins into smaller pieces. G protein-coupled receptors (GPCRs) already play a fundamental role in the regulation of various physiological and pathological processes.

One of the fragments that is produced following cleavage by the I?-secretase is the amyloid-I? peptide, which aggregates to form amyloid plaques. Our research indicates that the absence of GPR3 alleviates the cognitive decline and reduces amyloid pathology in multiple disease-relevant models.
Consequently, validation of AD therapeutic targets in multiple models is required prior to advancing to clinical research. The identification of GPR3 as an AD therapeutic target provides an important new perspective in AD drug development. The accumulation of amyloid plaques in the brains of Alzheimer's disease patients leads to the gradual degeneration of brain networks and disruption of mental function.

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