In a recent study published in IScience , a team of researchers from the United States examined the impact of heparan-sulfate-modified proteoglycans (HSPGs) on Alzheimer's disease-associated pathways in mitochondrial function, autophagy, and liposomes using mouse astrocytes and human cells. They also examined whether HSPG-mediated signaling modulations countered the effect of compromised presenilin function in Drosophila . Study: Altering heparan sulfate suppresses cell abnormalities and neuron loss in Drosophila presenilin model of Alzheimer Disease .
Image Credit: PopTika/Shutterstock.com Alzheimer's disease is characterized by three major histopathological features — amyloid plaques, neurofibrillary tangles, and adipose saccules or intracellular lipid accumulation in the glia. Most of the pharmaceutical strategies for developing Alzheimer's disease treatments have focused on these histopathological abnormalities, especially amyloid plaques, and some have been successful in slowing cognitive loss.
However, other cellular deficits are common to the early-onset, familial form of Alzheimer's disease and the late-onset form of the disease, with risk-associated variants identified through genome-wide association studies. Studies have identified modifications in genes involved in membrane trafficking, innate immunity, and cholesterol metabolism associated with Alzheimer's disease. In the present study, the researchers used mouse astrocytes and human cell cultures to examine the.