Why Alzheimer's patients have no memory loss when the disease starts?
Researchers at the University of Barcelona (UB) and the Institute for Bioengineering of Catalonia (IBEC), together with members of the CIBERNED at the Centre for Molecular Biology in Madrid, and the Institute of Neuropathology of IDIBELL - Bellvitge University Hospital, reveal that our nervous systemʼs naturally protective response to the onset of Alzheimer's may contribute to the fact that patients do not suffer memory loss until the disease has progressed further. The study has been published in the journal Molecular Neurobiology.
Researchers at the University of Barcelona (UB) and the Institute for Bioengineering of Catalonia (IBEC), together with members of the CIBERNED at the Centre for Molecular Biology in Madrid, and the Institute of Neuropathology of IDIBELL - Bellvitge University Hospital, reveal that our nervous systemʼs naturally protective response to the onset of Alzheimer's may contribute to the fact that patients do not suffer memory loss until the disease has progressed further. The study has been published in the journal Molecular Neurobiology.
Alzheimer's is a neurodegenerative disease characterized by a gradual loss of memory and other mental dysfunction, as neurons die and different areas of the brain atrophy. The disease is the most common form of dementia and appears most frequently in people over 65. There are two stages: the initial one where symptoms arenʼt clear, and a second phase with well-defined symptoms. Alzheimer's can be attributed to two major events that can happen in the brain: the presence of extracellular aggregates, mostly a compound known as beta-amyloid peptide, which forms plaques; and the accumulation of a very phosphorylated form of the protein tau, which forms small tangles inside affected neurons.
Researchers describe the relationship between beta-amyloid peptide oligomers and tau phosphorylation and the presence of another protein, the cellular prion protein (PrPc), in affected neurons. “Previous studies had looked at the levels of PrPc in advanced stages of the disease”, explains Dr José Antonio del Río, leader of the Molecular and Cellular Neurobiotechnology Research Group at IBEC and professor from the Department of Cellular Biology at UB. “Our new study —he points out— shows, both in mice and human brains affected by Alzheimerʼs, an increase in protein PrPc during the early, asymptomatic stages of the disease. However, these levels of PrPc decrease as the disease progresses”. “As a result, it is reasonable to draw the conclusion that the overexpression of PrPc seen at the beginning of the disease is part of the protective response of the nervous system in an attempt to suppress the progress of Alzheimerʼs”, concludes Dr del Río.