Alzheimer’s disease is the most common cause of dementia, accounting for approximately 70% of all cases (Plassman et al., 2007).
The remaining cases are accounted for by vascular dementia, Lewy body dementia, Parkinson's disease, frontotemporal dementia, and mixed dementia types (e.g., Alzheimer’s disease with Lewy body pathology and Alzheimer’s disease with vascular pathology; Livingston et al., 2017; Mahendra & Hopper, 2013; Plassman et al., 2007). See ASHA’s resource on
Most dementias are the result of neuropathology stemming from (a) diffuse degeneration in cortical and/or subcortical structures and neural pathways and/or (b) chemical changes that affect neural functioning.
Structural changes include neurofibrillary tangles and neuritic plaques—both commonly associated with Alzheimer's disease—and loss of neural pathways (connections between neurons) responsible for memory and new learning.
Chemical changes include (a) cholinergic deficits within the subcortical structures as in Alzheimer’s disease or (b) chemical imbalances associated with metabolic disorders.
A number of risk factors have been associated with dementia. Some are modifiable, and others are nonmodifiable.
Modifiable Risk Factors
Modifiable risk factors for dementia are those that, if eliminated, can potentially prevent some cases of dementia. Based on available data and models of dementia risk, Livingston et al. (2017) describe nine modifiable life-course risk factors for dementia. These factors are grouped below by age range across the lifespan.
Early life (< 18 years)
- Less education (none or primary school only)
Middle life (45–65 years)
- Hearing loss
Later life (> 65 years)
- Physical inactivity
- Social isolation
Based on their analysis, Livingston et al. (2017) estimate that about 35% of dementia can be attributed to a combination of these nine factors. Mechanisms that may be linked to these risk factors include vascular damage to the brain that increases the risk of vascular lesions, atrophy, and neurodegeneration; less available cognitive reserve (see “Reserve” subsection below); and metabolic changes that affect amyloid clearance. See Livingston et al. (2017) for details and summary.
Nonmodifiable Risk Factors
Nonmodifiable risk factors are those that cannot be changed or modified by the individual. They include age and heredity.
Age is the greatest nonmodifiable risk factor for dementia. Every 5 years after age 65, the number of individuals with Alzheimer’s disease doubles; about one third of people over age 85 have the disease (National Institute on Aging, 2017).
Heredity can play a part in dementia risk. For example, the risk of acquiring dementia is higher if an individual has a first-order relative with the disease (Green et al., 2002; Lovestone, 1999; Wolters et al., 2017). This risk may be linked to inheritance of the Apolipoprotein E (ApoE) gene (e.g., Green et al., 2002; Lovestone, 1999) or to unexplained hereditary causes (Wolters et al., 2017).
The concept of reserve was introduced to account for the observation that there does not seem to be a direct relationship between the amount of brain damage or pathology and the degree of disruption in performance (Stern, 2002, 2003, 2006, 2009). Reserve is applicable to most situations in which disruption to brain functioning occurs, including traumatic brain injury, stroke, and dementia. The concept is often used to explain differences in susceptibility to brain changes related to aging or Alzheimer’s disease (Livingston et al., 2017; Stern, 2012).
Models used to explain the concept of reserve fall into two general categories—passive and active. Passive models (Katzman, 1993; Satz, 1993) explain reserve in terms of “brain reserve capacity” (BRC) and include brain size and synapse count. There are individual differences in BRC such that, given the same brain damage or pathology, individuals with more BRC are less likely to manifest clinical deficits than are individuals with less BRC (Stern, 2003).
Active models (e.g., cognitive reserve [CR]) focus on how tasks are processed, rather than on physiologic differences in the brain itself (Stern, 2003, 2012). These models suggest that some individuals use neural networks or cognitive processing approaches that are more efficient and less susceptible to damage, or they use compensatory approaches not normally used prior to injury (Stern, 2002, 2009, 2012). Individual differences exist such that, given the same brain damage, those with greater CR are better able to cope than are those with less CR (Stern, 2012).
Factors that Affect Reserve
Lifestyle factors such as higher education, physical activity, intellectual stimulation, and social involvement are associated with lower risk of dementia. These factors are thought to increase reserve, which in turn increases capacity to cope with brain injury or pathology (e.g., Livingston et al., 2017; Stern, 2012).
In addition to lifestyle factors, lifelong bilingualism may also contribute to cognitive reserve (see Guzmán-Vélez & Tranel  for a review). In studies comparing bilingual and monolingual individuals, bilinguals demonstrated onset of dementia symptoms approximately 4–5 years later than monolinguals (Bialystok, Craik, & Freedman, 2007; Craik, Bialystok, & Freedman, 2010). The cognitive demands of bilingualism may contribute to increased cognitive reserve in much the same way as do other stimulating activities (Craik et al., 2010). These results cannot be generalized to individuals who are not fully bilingual (Bialystok et al., 2007).
Overall, 15% of the adult population in the United States age 18 and older report having some trouble hearing (Blackwell, Lucas, & Clarke, 2014). Self-reported hearing loss increases with age, with 5.5% of adults ages 18–39, 19% of adults ages 40–69, and 43% of adults over age 70 reporting difficulty hearing without a hearing aid (Zelaya, Lucas, & Hoffman, 2015).
Adjusting for other risk factors (e.g., education, diabetes, cardiovascular factors), studies show that hearing loss is independently associated with increased risk of dementia (Deal et al., 2017; Lin et al., 2011). For individuals over 60 years of age, more than one third of the risk of all-cause dementia was found to be associated with hearing loss (Lin et al., 2011).
Further, individuals with baseline hearing loss were found to have greater rates of cognitive decline over time than individuals with normal hearing (Lin et al., 2013), and the mean time to develop dementia was reported to be faster for individuals with self-reported hearing loss than for individuals without self-reported hearing loss (Gurgel et al., 2014).
Several hypotheses have been proposed to account for the association between hearing loss and dementia. They include the following:
- Common cause hypothesis—suggests that hearing loss and dementia share the same etiology (neural degeneration associated with aging), but one does not cause the other (Baltes & Lindenberger, 1997; Lindenberger & Baltes, 1994).
- Cascade hypothesis—suggests that sensory deprivation (secondary to hearing loss) leads directly to impoverished cortical sensory input and indirectly to social isolation and depression, both of which in turn lead to cognitive decline (see, e.g., Baltes & Lindenberger, 1997; Lindenberger & Baltes, 1994; Stahl, 2017; Tun, McCoy, & Wingfield, 2009).
- Cognitive load hypothesis—suggests that when hearing loss is present, greater cognitive resources are dedicated to auditory processing, leaving fewer resources for other cognitive processes like working memory that are involved in the processing and comprehension of speech (see, e.g., Baltes & Lindenberger, 1997; Lindenberger & Baltes, 1994; Martini, Castiglione, Bovo, Vallesi, & Gabelli, 2014; Peelle, Troiani, Grossman, & Wingfield, 2011).
It is possible that the mechanism proposed by each of these hypotheses is not mutually exclusive, and that each contributes individually or in combination to increase the risk of dementia. Further investigation is needed to clarify the relationship between hearing loss and dementia (Loughrey, Kelly, Kelley, Brennan, & Lawlor, 2018; Thomson, Auduong, Miller, & Gurgel, 2017).