Most dementias are the result of neuropathology resulting from diffuse degeneration in cortical and/or subcortical structures and neural pathways, and/or chemical changes that affect neural functioning. Examples of structural changes include neurofibrillary tangles and neuritic plaques, commonly associated with Alzheimer's disease. Neural pathways (connections between neurons) responsible for memory and new learning are also lost. Examples of chemical changes include cholinergic deficits within the subcortical structures, as in Alzheimer's disease, or chemical imbalances associated with metabolic disorders.
Alzheimer's disease is the most common cause of dementia, accounting for approximately 70% of all cases (Plassman et al., 2007), and the risk of acquiring Alzheimer's is higher if an individual has a first-order relative with the disease (Lovestone, 1999). Vascular dementia is widely considered the second most common cause, accounting for approximately 17% (Plassman et al., 2007). The remaining cases are accounted for by dementia with Lewy bodies, Parkinson's disease, frontotemporal lobar dementia, and mixed dementia types (e.g., AD with Lewy body pathology and AD with vascular pathology; Mahendra & Hopper, 2013; Plassman et al., 2007).
The concept of cognitive reserve was introduced to account for the observation that there does not appear to be a direct relationship between the severity of brain damage or pathology and the degree of disruption in performance (Stern, 2003, 2009). It is applicable to most situations in which disruption to brain functioning occurs, including traumatic brain injury and dementia.
Models of cognitive reserve postulate that increased brain reserve capacity (e.g., brain size or synapse count; Satz, 1993) or more efficient cognitive processing (Stern, 2002) allows some individuals to cope with brain insult better than others. Individual differences in cognitive reserve can stem from genetic differences or differences in life experiences, including educational and occupational experiences and involvement in leisure activities (Stern, 2009).
In addition to lifestyle factors, lifelong bilingualism has been proposed as a factor contributing to cognitive reserve. In studies comparing bilingual and monolingual individuals, bilinguals demonstrated onset of dementia symptoms approximately 4 to 5 years later than monolinguals (Bialystok, Craik, & Freedman, 2007; Craik, Bialystok, & Freedman, 2010). The cognitive demands of bilingualism may contribute to an increased cognitive reserve in much the same way as other stimulating activities (Craik et al., 2010). These results cannot be generalized to individuals who are not fully bilingual (Bialystok et al., 2007).