One of the things that makes Alzheimer's disease difficult to diagnose is the existence of symptomatic and not symptomatic versions. Despite having the same genetic variants and similar neurological conditions, some patients exhibit different levels of cognitive decline.
According to a study by the University of California, the phenomenon could be linked to the interaction of certain proteins. Family Alzheimer's has a strong genetic component, but the most common is sporadic Alzheimer's. Little is known of the latter. Its risk factors include age, gender and family history. However, social and biological factors that stimulate the accumulation of amyloid proteins also appear to contribute. By accumulating, the proteins form plaques that kill neurons and cause the typical symptoms of the disease.
The researchers studied 414 cases of diagnosed Alzheimer's, comparing it to a healthy control group. In doing so they went beyond genetic analysis and also analyzed the sum of mRNA molecules. From what has emerged, the presence or absence of interactions between proteins can modify how genes express themselves and how the disease evolves. Depending on the groups of genes involved, synaptic transmission and cellular metabolism also change. All critical aspects for sporadic Alzheimer's disease.
The discovery could facilitate early diagnosis of the disease, one of the biggest problems at the moment. A better understanding of how genes are linked and how proteins affect them, in fact, could help to develop tests to be used before the symptomatic phase.