Dysfunctional Autophagy in an Alzheimer ' s Disease Model Unexpectedly Results in Lower Levels of Amyloid- β

Cell biology is complicated, to say the least, and so the unexpected keeps occurring. Autophagy is a collection of cell maintenance mechanisms responsible for clearing out broken structures and unwanted proteins within cells. There is plenty of evidence for its role in policing aggregates such as the amyloid-β associated with Alzheimer's disease. It is suspected that the faltering of autophagy that occurs with age is one the reasons why neurodegenerative conditions like Alzheimer's disease are a feature of late life only. Here, researchers undertake a routine study of dysfunctional autophagy in Alzheimer's disease. They break the normal operation of autophagy via the use of mice with a mutant ubiquitin gene, and cross those mice with an Alzheimer's model lineage to obtain mice that exhibit both amyloid-β and broken autophagy. The expected result was a much more rapid accumulation of amyloid-β, as autophagic processes would fail to clear unwanted protein aggregates, but in fact exactly the opposite occurred. Sadly, the animal models of Alzheimer's disease are highly artificial constructs, as humans are near the only species in which this condition occurs. So it is hard to say whether this has any relevance to Alzheimer's disease in humans, or whether it is a peculiar artifact of the model. This has long been a major challenge in this field of research, the sizable gap between the animal models and the real thing, much larger than is the case for other conditio...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs