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A protein that protects the brain from Alzheimer’s – scientists

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It reduces amounts of amyloid protein, which produces senile plaques, and it was discovered recently.

Every three seconds, someone in the world succumbs to dementia. More than half a million people in the United States have Alzheimer’s disease, which is a leading cause of dementia and disability among the elderly. Nearly 200,000 scientific books have been published since Alois Alzheimer first described this terrible disease in 1903, with nearly 3,500 published in the last few months.

The most recent research from this group has found that a little-known protein called LRP3 regulates the amounts of amyloid beta, the protein that builds up in the brain of persons with Alzheimer’s disease and forms the plaques that characterize the condition. Dr. Inmaculada Cuchillo-Ibañez is the first author of the study, which was published in the journal Alzheimer’s Research & Therapy.

A protein that protects the brain from Alzheimer's - scientists
Study finds a protein that protects the brain from Alzheimer’s

When the scientists investigated the role of LRP3, which was previously unknown, they discovered that it had a significant impact on the amounts of amyloid precursor protein (APP). The small protein -amyloid, which makes up the majority of the plaques observed in the brains of persons with Alzheimer’s disease, gives APP its name. An increase in LRP3 levels would be helpful, and since it can modulate the amounts of APP and -amyloid, it could be an entirely new path for Alzheimer’s research, according to the study authors.

NEUROPROTECTION LOSS

The study looked at the expression of LRP3 in healthy middle-aged adults and those with Alzheimer’s disease using human frontal brain tissues from the Neuropathology Institute at the Bellvitge University Hospital’s Tissue Bank.

They discovered that the levels of LRP3 in the brains of Alzheimer’s patients were lower at the start of neurodegeneration. In other words, they may lose LRP3’s protective role in relation to β-amyloid levels at the onset of dementia, which could be a burden as the disease progresses, because the ability to reduce β-amyloid levels and, therefore, control the existence of senile plaques in the brain, is lost from the start, says the lead author.

LRP3 is a receptor that can bind to the protein apoE. Late-onset Alzheimer’s disease is linked to the gene that produces apoE. (onset after 65 years). The apoE protein comes in three different forms: apoE2 (the least prevalent in humans), which lowers the risk of Alzheimer’s, apoE3, the most frequent form, which has no effect on the chance of developing the disease, and apoE4, which is linked to a higher risk of developing the disease.

The researchers also revealed that ApoER2, a receptor present in the membrane of neurons like LRP3, promotes the increase in LRP3 levels and hence its role as a regulator of amyloid plaque formation in the brain. LRP3 and ApoER2 are low-density lipoprotein (LDL) receptors that mediate lipoprotein uptake and have traditionally been researched for their role in cholesterol transport and metabolism. As apolipoprotein E (ApoE) receptors, members of the LDL receptor family are known to have a role in the control of synaptic plasticity and the development of Alzheimer’s disease.

The discovery of LRP3’s presumably neuroprotective function by researchers at the Institute of Neurosciences has opened up a new avenue of research that could lead to the discovery of new, more effective therapeutic targets for modifying or stopping the progression of Alzheimer’s disease, which is an important goal that has yet to be achieved.

“Our interest now is precisely the relationship between ApoE and LRP3. We know that ApoE4 is a risk factor for Alzheimer’s and it would be interesting to find out its relationship with LRP3 and, indirectly, its effect on APP and β-amyloid levels. Every person has one of the forms of ApoE, either ApoE2, ApoE3, or ApoE4, but we all have LRP3, so finding out the relationship between the different forms of ApoE and LRP3 is very important because really the effect that we see of LRP3 on APP and the β-amyloid protein is quite drastic and the levels of these two key proteins in the development of Alzheimer’s disease decrease a lot,” explains Dr. Cuchillo.

TAU, THE CONTROL POINT

Another promising route, according to Dr. Inmaculada Cuchillo, is to investigate the interaction between LRP3 and tau, another protein involved in the development of Alzheimer’s disease that produces neurofibrillary tangles.

“Until now, the relationship between tau and beta-amyloid protein in Alzheimer’s has been studied, but nothing has been advanced in terms of new therapies. We know that tau is an important protein for anchoring receptors to the cell membrane, and LRP3 is a cell membrane receptor. If we manage to identify the intermediate molecule between Tau and LRP3, perhaps we will open a new avenue of research because the future of Alzheimer’s research lies in opening new avenues that relate what we already know with what has just been discovered,” said the authors.

Source: 10.1186/s13195-021-00921-5

Image Credit: Getty

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