The combination of age-related cognitive decline and neurological damage sustained during a brain injury has a cumulative effect and produces profound deficits in older adults. The literature on cognitive decline following TBI in older adults is limited. In studies directly assessing older adults following a TBI, cognitive impairments have been found including delayed recall (Gupta & Ghai 1991) and word fluency (Aharon-Peretz et al. 1997).
Short-term and long-term cognitive decline have been shown to be a risk factor for older adults who have sustained a TBI; however, many older individuals experience a decline in cognitive functioning as a result of normal aging or pathology. Such pathology may include dementia, a progressive neurodegenerative disease whereby memory and thinking become impaired. There are currently 564,000 Canadians living with dementia, the majority of these individuals are over the age of 65, therefore, teasing apart the relationship between aging, TBI and dementia can be a difficult task for primary health providers (Chambers et al. 2016). Quite often dementia (un-related to a TBI) and TBI-related cognitive decline exist as co-morbid conditions. Typically individuals post TBI recover to some degree over time or plateau, whereas patients with dementia experience a progressive decline (Kersel et al. 2001). For example, compared to individuals with Alzheimer’s disease, individuals with TBI were able to learn new information and retain it over time with practice (Bigler et al. 1989) and perform better on both verbal and visual memory tests (Bigler et al. 1989; Goldstein et al. 1996). Determining whether dementia is the underlying problem as opposed to TBI sequela is made more challenging by the fact that a brain injury is a risk factor for developing Alzheimer’s disease and other dementias (Mortimer et al. 1991; Roberts et al. 1991; van Duijn et al. 1992; Mayeux et al. 1995; Plassman et al. 2000; Guo et al. 2000; Fleminger et al. 2003). Starkstein & Jorge (2005) claimed that the changes in the brain following TBI may lower the threshold for the manifestation of Alzheimer’s disease in predisposed individuals.
Protein upregulation and genetic factors may also contribute to neurodegeneration following a brain injury. Evidence has been accumulating over the past decade that the genetic polymorphism Apolipoprotein E (apoE protein; APOE gene) may play a role in cognitive outcomes after brain injury. In individuals post injury, the APOE4 allele has become an excellent predictor for poor clinical outcome, both physically and cognitively (Nicoll et al. 1996; Jordan et al. 1997; Teasedale et al. 1997; Friedman et al. 1999; Liaquat et al. 2002; Lynch et al. 2002; Starkstein & Jorge 2005; Swan et al. 2005; Blacker et al. 2007).
Age-related cognitive decline and neurological damage resulting from a brain injury have a cumulative negative effect and may produce cognitive deficits.
Cognitive impairment pathologies such as dementia (unrelated to a TBI) and TBI related cognitive decline often exist as co-morbid conditions among older adults.
The APOE4 allele is an independent predictor for poor clinical outcome, both physically and cognitively.