Claims for treatment for Alzheimer's have reached an impasse after successive failures in recent years, suggesting that we may need to think about some hypotheses about this common form of dementia.
Much of the focus in previous studies is focused on the accumulation of proteins, as they are directly responsible for the gradual loss of brain function.
For more than 100 years, German neurologist and neurologist Alois Alzheimer has reported the presence of plaques in the patient's brain with Alzheimer's disease. This resulted in the detection of an amyloid precursor protein (APP), which produces amyloid plaques or plaques in the brain suspected of Alzheimer's disease.
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Since then, proteins of amyloid precursors have been widely studied for their association with Alzheimer's disease. However, the distribution of these protein internal and external neurons and their function in these cells remains unclear.
A team of neuroscientists led by the University of Florida at the University of Florida at the University of Florida asked a fundamental question in their quest to fight Alzheimer's disease: "Are amyloid precursor proteins planned for Alzheimer's disease or just a partner?"
Mutations in amyloid previous proteins have been associated with rare cases of hereditary Alzheimer's disease.
Although scientists have gained a lot of knowledge about how the protein turns into amyloid plaques, they little know about its original function in neurons.
In the most common intermittent Alzheimer's disease, a greater risk factor is the protein involved in the transportation of cholesterol, and not the protein of this amyloid precursor. In addition, many clinical trials designed to treat Alzheimer's have failed to reduce the formation of amyloid plaques, including a Biogen experiment released last month.
In a new study published in the journal Neobobiology of Disease, lead author of the study, Qi Chang, Ph.D. Institute of Brain Sciences, Associate Professor at the University of Florida at the University of Florida at the Atlantic University, and associates from Vanderbilt University in Tennessee, Follow movements and changes in amyloid previous protein molecules, using quantum images with precision unprecedented.
It is surprising that, by separating the two, the researchers found that this manipulation not only impairs the movement of amyloid previous proteins, but also spoils the distribution of cholesterol on the surface of the neurons.
"Our study is interesting because we have noticed a strange relationship between amyloid precursor protein and cholesterol in the cellular membrane of nerve constraints, which are points of contact between neurons and the biological basis of learning and memory," said Zhang.
"The myeloid precursor protein can be only one of the many factors that help partially contribute to the reduction of cholesterol, and it's strange that the heart and brain are again encountered in the fight against bad cholesterol," he said.
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