ABSTRACT
It is widely recognized that individuals show varying degrees of susceptibility to cognitive and functional impairment associated with neurodegenerative disease or acquired brain injury. Although two individuals may suffer a similar neurological insult, underlying neuropathologies may produce profound clinical impairment in one individual but minimal or no impairment in the other. The theory of cognitive reserve (CR) was proposed to explain variations in symptom presentation among individuals with similar types and degrees of brain damage (Stern, 2002; 2003). The CR hypothesis posits that certain genetic and experiential variables protect against the expression of cognitive and functional impairment subsequent to brain injury or degenerative process, and an individual's reserve determines his or her threshold for the clinical manifestation of symptoms. CR therefore partially mediates the association between brain injury and its expression, such that individuals with high CR are able to tolerate a greater degree of neuropathology than are those with low CR prior to the onset of symptoms (Stern, 2002).
