Elsevier Logo A commonly run notion claims that family history of Alzheimer’s disease (AD) heightens chances to develop the disorder. If this piece of investigation is to be believed then, this link is stronger from the mothers’ side. A groundbreaking study claims that specific biological and genetic mechanisms increase risk of being diagnosed with AD. It was suggested that novel medications declining the threats associated with a maternal history of Alzheimer’s disease can be developed.

Genomic imprinting appears as a crucial phenomenon in which the pattern of AD differs based on whether the risk genes are inherited from the mother or the father. Imprinting, a form of epigenetic regulation allegedly causes long lasting alterations in gene function and is produced through regulatory mechanisms. During the investigation, experts examined Alzheimer’s risk in healthy, cognitively normal individuals by measuring their cerebrospinal fluid proteins. Apparently these fluid proteins change in Alzheimer’s. The results of individuals with a maternal or paternal Alzheimer’s history were then compared to those with no family history.

Dr. Lisa Mosconi, the first investigator on the research, shared, “Our data indicate that adult children of mothers with Alzheimer’s may be at increased risk for developing the disease. It is therefore extremely important to understand the genetic mechanisms involved in maternal transmission of Alzheimer’s disease, which are currently unknown. Identifying a genetic predictor for the disease might lead to preventive treatments years before the onset of clinical symptoms.”

The outcome was that participants whose mothers had Alzheimer’s registered altered levels of the amyloid protein. This protein seems to a hallmark for detecting the presence of AD. On the other hand, those with fathers suffering from AD and individuals with no family history had protein levels within normal range. Additional follow-up research is essential to ascertain the effectiveness of protein measures in suspecting vulnerability to AD.

The research is published in Biological Psychiatry.