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Researchers at the University of Texas Southwest have recently discovered that in a mouse model of Alzheimer’s disease, altering the biochemical properties of some brain cells can prevent the formation of beta amyloid plaques
Joachim Herz, the co-corresponding author of the study and a professor of molecular genetics and neurology at the University of Texas Southwest, said: "We expect that these drugs that work in mice will one day also be used in Alzheimer’s disease patients.
Nearly 6 million Americans suffer from Alzheimer's disease (AD), most of which are late-onset, that is, symptoms of dementia appear after the age of 65
Although the cause of this disease is not clear, scientists have found that the main genetic risk factor for late-onset Alzheimer's disease is apolipoprotein E4 (ApoE4)
The three versions of ApoE are very similar in structure
In this new study, Dr.
The researchers used genetically modified mice to simulate Alzheimer’s disease and produce human forms of ApoE4 and beta amyloid.
However, when the researchers used genetic technology to turn off a gene called NHE6 in brain cells, they found that the negative effects of ApoE4 were eliminated
"The protective effect of inhibiting NHE6 is the same as that of ApoE2, and we hope that this effect can eventually be reproduced with drugs," the researchers said
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NHE6 depletion corrects ApoE4-mediated synaptic impairments and reduces amyloid plaque load
eLife 2021;10:e72034 DOI: 10.
