The study reveals that introducing progerin, a protein associated with accelerated aging, into cellular models of Alzheimer's Disease (AD) can hasten the development of AD-related traits. This innovative approach offers a more efficient method for studying AD mechanisms, potentially accelerating the discovery of new treatments.
By Dr. Priyom Bose, Ph.D.Oct 31 2023Reviewed by Benedette Cuffari, M.Sc. The pathogenesis of Alzheimer’s Disease , a leading cause of dementia, remains unclear. One notable limitation of current cellular models is that they lack an aging in vitro environment.
Study: Development of an accelerated cellular model for early changes in Alzheimer’s disease. Image Credit: unoL / Shutterstock.com AD can categorized as FAD, which begins before an individual turns 65, or sporadic AD , which generally occurs after the age of 65 years. Neurofibrillary tangles comprising tau protein and senile plaques consisting of β-amyloid are features of AD.
Related StoriesTo this end, human neural progenitor cells were extracted from the ventral mesencephalon region of human fetal brains. For lentivirus packaging and transduction, HEK293T cells were co-transfected with two virus packaging vectors and lentiviral plasmids. These observations imply that the expression of progerin or lamin A could lead to aging, thereby increasing the risk of disease development. More specifically, progerin expression accelerated the development of AD phenotypes to three to four weeks from eight to 16 weeks.
This is crucial because, for neighboring cells, it offers an aged microenvironment. Thus, neighboring cells become more vulnerable and may eventually die.
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