Purpose of review
Despite signs of cortical and subcortical loss, patients with prodromal and early-stage neurodegenerative disease are able to perform at a level comparable to the normal population. It is presumed that the onset of compensatory processes, that is changes in brain activation within a function-specific network or in the recruitment of a region outside of the task-network, underlies this maintenance of normal performance. However, in most studies to date, increased brain activity is not correlated with indices of both disease and performance and what appears to be compensation could simply be a symptom of neurodegeneration.
MRI studies have explored compensation in neurodegenerative disease, claiming that compensation is evident across a number of disorders, including Alzheimer's and Parkinson's disease, but generally always in early stages; after this point, compensation is generally no longer able to operate under the severe burden of disease. However, none of these studies explicitly adopted a particular model of compensation. Thus, we also discuss our recent attempts to operationalize compensation for empirical testing.
There is clear evidence of compensatory processes in the early stages of neurodegenerative disease. However, for a more complete understanding, this requires more explicit empirical modelling.