Using the PHD 7 mer library to analyze CSF tau concentrations in Alzheimer's Disease and control patients

Alzheimer’s disease (AD) is the 6th leading cause of death in the United States and primarily affects those 65 and older. AD is pathologically defined by the existence of amyloid plagues composed of the b-amyloid(Ab), peptide and neurofibrillary tangles composed primarily of the microtubule-associated protein tau. Because age is the number one risk factor to get AD, the prevalence is only expected to increase as life expectance continues to rise1. Those who are clinically diagnosed with AD have a decrease in cognitive function as well as other behavioral deficits such as agitation. While clinical trials are ongoing, no new therapies to prevent or reverse AD progression have been found. Lack of pharmalogical success is thought to be because clinical intervention happens too late in the disease course and neuronal damage is too severe. Therefore, there has been a shift in focus within within the field to find biomarkers to indicate early neuronal changes. A putative biomarker is the tau protein, as it functions in microtubule formation and stabilization and neuronal structural integrity. We hypothesize that the absence or presence of posttranslational modifications (PTMs) in tau may indicate AD’s progression in patients through the “gain of toxic function2.” Using PTM changes in tau as biomarkers allows for an early diagnosis in advance to the beginning of symptoms commonly related to Alzheimer’s disease.
Download pdf
Abstract/Description: Alzheimer’s disease (AD) is the 6th leading cause of death in the United States and primarily affects those 65 and older. AD is pathologically defined by the existence of amyloid plagues composed of the b-amyloid(Ab), peptide and neurofibrillary tangles composed primarily of the microtubule-associated protein tau. Because age is the number one risk factor to get AD, the prevalence is only expected to increase as life expectance continues to rise1. Those who are clinically diagnosed with AD have a decrease in cognitive function as well as other behavioral deficits such as agitation. While clinical trials are ongoing, no new therapies to prevent or reverse AD progression have been found. Lack of pharmalogical success is thought to be because clinical intervention happens too late in the disease course and neuronal damage is too severe. Therefore, there has been a shift in focus within within the field to find biomarkers to indicate early neuronal changes. A putative biomarker is the tau protein, as it functions in microtubule formation and stabilization and neuronal structural integrity. We hypothesize that the absence or presence of posttranslational modifications (PTMs) in tau may indicate AD’s progression in patients through the “gain of toxic function2.” Using PTM changes in tau as biomarkers allows for an early diagnosis in advance to the beginning of symptoms commonly related to Alzheimer’s disease.
Subject(s): Undergraduate Research
Alzheimer's Disease (AD)
PTM changes