Apolipoproten E (apoeE) is a major genetic risk factor for the development of Alzheimer’s disease, yet the protein tends to be understudied as a potential druggable target for the mind-robbing neurodegenerative disease.
Apolipoproten E (apoeE) is a major genetic risk factor for the development of Alzheimer’s disease, yet the protein tends to be understudied as a potential druggable target for the mind-robbing neurodegenerative disease.
Now a research team led by the University of South Florida Health (USF Health) Morsani College of Medicine reports that a novel apoE antagonist blocks apoE interaction with N-terminal amyloid precursor protein (APP). Moreover, this peptide antagonist, known as 6KApoEp, was shown to reduce Alzheimer’s-associated beta amyloid (β-amyloid) accumulation and tau pathologies in the brain, as well as improving learning and memory in mice genetically engineered to mimic symptoms of Alzheimer’s disease.
Many failed anti-amyloid therapies for Alzheimer’s disease have been directed against various forms of the protein β-amyloid, which ultimately forms clumps of sticky plaques in the brain. The presence of these amyloid plaques is one of the major hallmarks of Alzheimer’s disease.
The USF Health research findings suggests that disrupting apoE physical interaction with N-terminal APP may be a new disease-modifying therapeutic strategy for this most common type of dementia.
Read more at: University of South Florida
Study lead author Darrell Sawmiller, PhD (left), and senior author Jun Tan, PhD, MD (Photo Credit: University of South Florida)
