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USF researchers confirm the effectiveness of an antagonist of apoE
Alzheimer's disease is the most common degenerative brain disease that causes dementia, often called senile dementia.
Along with the advent of an aging society, the rate of patients with Alzheimer's disease is also increasing.
It is estimated that there are only 5.8 million inhabitants in the United States and more than 50 million worldwide.
However, no treatment has been developed to prevent or stop this terrible disease.
The researchers reported that antagonists of apolipoprotein E (apoE), a major genetic risk factor for Alzheimer's disease, alleviate the symptoms of Alzheimer's disease.
This antagonist blocks the interaction of apoE with the precursor protein of N-terminal amyloid (APP).
Apolipoproteins are clbadified into more than 10 species depending on the density and synthetic tissue of the lipoprotein present.
ApoE binds to low density lipoprotein (LDL) receptors and is produced in the liver.
Jun Tan, professor of psychiatry and behavioral neuroscience at the University of South Florida's (USF) School of Medicine, recently published a report on this study in the journal Biological Psychiatry.
13 (local time) online (link [http://www.eurekalert.org/pub_releases/2019-06/uosf-rdp061219.php]According to a press release published in the press release, Tang's team discovered in the brain a 6KApoEp antagonist that attenuated beta-amyloid deposition and the pathological effects of tau protein.
The researchers found that 6KApoEp was administered to mice with Alzheimer's disease because of genetic engineering techniques, thus enhancing their learning and memory abilities.
Antagonists are substances that interfere with the metabolism of other substances with similar molecular structures.
Amyloid is a fibrous aggregate formed by the accumulation of several proteins. It is linked to certain types of human diseases, including certain neurodegenerative diseases.
In particular, beta-amyloid, with tau protein, is considered the agent responsible for Alzheimer's disease.
Although there have been numerous attempts to eliminate amyloid beta from the brain of patients with Alzheimer's disease, it was difficult to determine the therapeutic target among the various forms of Alzheimer's disease. amyloid beta.
In this regard, the study suggests that blocking the interaction of apoE with the N-terminal APP could constitute a new "disease-modifying" treatment strategy for the disease of D & D. # 39; Alzheimer's.
The N-terminus refers to the amino group of two amino acids located at both ends when several amino acids form a polypeptide by means of a peptide bond.
The amino acid at the other end of the carboxyl group is called C-terminal.
"We sought to pathologically identify how apoE and APP interacted and led to the formation of beta amyloid plaques and neuronal cell loss," said Dr. Tan, lead author of the report. "We have discovered a derivative of apoE that regulates the neuropathological phenomenon."
/ News Yonhap
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