Cognitive Health for an Aging Population

Laura A. Stokowski, RN, MS


November 16, 2009

In This Article

Cognition and the Aging Brain

At the heart of the issue is whether it is possible for the brain to stay young as the body grows old. To understand how aging transforms the brain, and whether these effects are permanent or modifiable, we must also ask:

  • How does the brain "normally" age?

  • What is cognitive decline, and how does it differ from cognitive impairment, AD, and dementia?

  • When does cognitive decline begin?

  • What is cognitive health?

  • Are there risk factors for cognitive decline or protective factors for cognitive health?

How Does the Brain Normally Age?

No operational definition of "normality" in the aging brain exists, which greatly restricts our ability to distinguish normal from abnormal age-related cognitive function.[3] Large interindividual differences in functional and structural elements of brain aging complicate matters further.[4,5]

The brain naturally undergoes gradual structural and functional changes, even in the absence of neurodegenerative disease.[6] Shrinking brain parenchyma, especially in the frontal regions, can result in 10% loss of brain volume after age 80, with concomitant reductions in cerebral blood flow and levels of chemical neurotransmitters. Senile plaques and neurofibrillary tangles (the hallmarks of AD) can accumulate in the normally aging brain, although they are much greater in number and distribution in the AD brain.[7]

On the positive side, the adult brain is capable of a greater degree of plasticity than scientists have previously believed. Evidence of brain resilience includes amelioration of age-related deterioration and successful cortical remodeling in the elderly brain.[5] Neurogenesis can, and does, persist into the 8th decade of life, even in the brain regions involved in learning and memory.[8] It seems that you can teach an old dog new tricks, and he or she can remember them.

Cerebral blood flow studies have identified patterns of age-related functional decline in multiple brain regions of otherwise healthy elderly individuals.[9] At the same time, increased activity in some brain regions suggests that the brain undergoes cortical reorganization with advancing age; in essence, the brain reorganizes itself, perhaps as a way of compensating for declining function. Because these changes can occur in the absence of declining performance, this may represent compensation in the healthy aging brain.[9] Alternatively, in some people, cortical recruitment could be an early compensatory response by the brain to maintain performance in the initial stages of AD.[10]

What Is Cognitive Decline?

Cognitive decline is a term -- along with cognitive impairment, AD, and dementia-- often used in discussions about cognition and aging. Molly Wagster, PhD, Chief, Behavioral & Systems Neuroscience Branch and Division of Neuroscience of the National Institute on Aging, explains the differences, starting with what happens to cognitive abilities as we age.

"A whole host of abilities, such as language, memory, and reasoning, fall under the domain of cognition. As we age, there are changes in cognitive function, accompanied by behavioral changes, that are independent of pathology or disease. Just as you wouldn't say that a marathon runner who slows down in his eighties has a motor disease, age-related cognitive decline isn't necessarily pathological. We may just be slower to retrieve information, and slower to learn new things. A wide variety of performance changes accompanied by a wide range in type and degree of cognitive changes all fall within the normal limits of cognitive aging. And age-related cognitive changes aren't necessarily all negative -- increased vocabulary, depth of comprehension, and accumulating wisdom can all compensate for less positive effects of aging."

Wagster differentiates common age-related cognitive decline from a specific condition called mild cognitive impairment (MCI). Individuals with MCI have an impairment of memory that is evident to others, although the individual can still perform most activities of daily living (eg, balance a checkbook, drive a car). When memory is the only cognitive domain affected, this condition is called MCI of the amnestic type and is characterized by subjective and objective memory loss, but not necessarily by functional disability. Some experts believe that MCI represents a transitional stage between normal aging and AD[11] and is a precursor to dementia. Indeed, Alzheimer's disease will develop in 12% of patients with MCI within a year's time.[12]

Others maintain that cognitive impairment actually represents early dementia. Roughly 22% of people age 71 years or older have cognitive impairment without dementia.[13] Mild impairments in other areas of cognition, such as executive functions (planning and carrying out tasks, abstract thinking, flexibility, decision-making, etc.), have also been recognized.[14] Cognitive impairment associated with chronic medical conditions accounts for 24% of cognitive impairment without dementia and may be the most underdiagnosed subtype of cognitive impairment without dementia.[13]

Dementia is the development of cognitive deficits that include memory impairment and at least one other cognitive disturbance (eg, difficulty with language, impairment in executive function). Dementia is a primary clinical feature of many disorders and may manifest as dementia of the Alzheimer's type, vascular dementia, Lewy body dementia, dementia associated with infectious disease (eg, Creutzfeldt-Jakob disease),dementia associated with various medical conditions, and others.[15] Different types of dementia have distinct symptom patterns and distinguishing microscopic brain features. However, considerable overlap seems to typify the dementias, making them difficult to sort out.[11] Some are treatable, and some are not.

AD is the most common form of dementia. The distinction between age-typical cognitive decline and AD is that AD involves not only memory loss, but also actual damaged brain cells with associated behavioral changes and deteriorating global functioning in activities of daily living. Affected individuals may be unable to learn, comprehend, or retain new information, and may exhibit limitations in verbal expression. They may be unable to think abstractedly, make sound judgments, or carry out complex tasks. AD has early and late onset forms. Although AD has been the focus of much research, it is still unknown whether late-onset AD represents an acceleration of the progressive memory loss associated with normal aging, or whether it is a distinct disease entity.[10]

The societal and financial burden of AD is already high and is rising. AD is now the 6th leading cause of death[16] and deaths from this incurable disease have risen while deaths from coronary disease and cancer have declined. AD triples healthcare costs for Americans 65 and older.[16] AD is not a disease of individuals, but of families, because persons affected by AD require more assistance with basic activities of daily living and usually can't live independently. For the 5.3 million people already living with AD (a new case every 70 seconds), 9.9 million unpaid caregivers are taking care of them.[16] These sobering figures will increase dramatically in the near future, and the social and financial tolls will be incalculable. An all-inclusive account of the Alzheimer crisis in the United States can be found in the Alzheimer's Study Group report.[17]

When Does Cognitive Decline Begin?

This question is important to the design of interventions to prevent or reverse cognitive decline, but the answer depends on who you ask. Evidence from cross-sectional research supports the theory that cognitive performance and neurobiological variables believed to affect cognition begin with minute but measureable declines in early adulthood (late 20s and early 30s). In contrast, some longitudinal studies suggest that cognitive abilities are stable until much later in life (50s, 60s, or even later). Salthouse[18] proposes that a major shortcoming of the longitudinal design (retesting the same individual) can distort the results of these studies; others believe that longitudinal studies can assist in determining causation.[19]

If cognitive decline does begin, however incrementally, as soon as a person reaches maturity, then we are waiting far too long to promote cognitive health. Cognitive health should not be considered separately from other aspects of physical health, and public education must be targeted to a much younger population.

What Is Cognitive Health?

Cognitive health as it pertains to the elderly should be defined "not just as the absence of disease, but rather as the development and preservation of the multidimensional cognitive structure that allows the elderly to maintain social connectedness, an ongoing sense of purpose, and the abilities to function independently, to permit functional recovery from illness or injury, and to cope with residual functional deficits."[19]

The 9 elements of cognitive health are: language, thought, memory, executive functions, perception, judgment, attention, remembered skills (such as driving), and the ability to live a purposeful life. Preserving these functions can literally make the difference between leading an independent or a dependent life.[20]

Emotional health is just as important as cognitive health.[21] Like cognitive health, emotional health is not simply the absence of psychiatric illness, but the presence of positive emotional adaptation in areas such as emotional regulation (the ability to control one's emotions) and emotional intelligence (the ability to use and identify emotions constructively).[21] Emotional health comprises personal traits that promote successful adaptation, such as resilience, mastery, self-efficacy, and wisdom. Self-efficacy and the ability to engage with others may ward off the sadness and depression that often characterize old age and speed cognitive decline.[21]

What Are the Risk Factors for Cognitive Decline and the Protective Factors for Cognitive Health?

Risk Factors. Advancing age is the most important risk factor for cognitive decline, cognitive impairment, and dementia. Significant associations also exist between cognitive decline and both physical inactivity and vascular disease. The link between hypertension in midlife and later cognitive decline is particularly strong.[22] Cardiovascular disease increases the risk for severe and permanent neurologic deficits. Controlling the risk factors for heart disease (hypertension, smoking, obesity, lack of exercise) may slow the process of cognitive decline, but it is not yet known whether such changes can actually improve cognitive function.[23]

In a recent extensive literature review, a broad range of factors were found to be associated with poor cognitive outcome. The most consistent were increasing age, hypertension, diabetes, stroke or transient ischemic attacks, infarcts or white matter lesions in brain imaging, higher body mass index (BMI), biological markers of inflammation, and depressed mood.[19] Poor emotional health (associated with functional/physical disability), chronic illness, sensory handicaps, stress, female sex, and personality characteristics such as neuroticism are risk factors for poor emotional outcome.[19] In single studies, other factors significantly related to poor cognitive outcomes were exposure to lead, alcoholism, insufficient sleep, cancer, and osteoporosis. It is also possible that other still unidentified medical, biological, or social/lifestyle factors are responsible for the differences in individuals who follow different cognitive trajectories as they age. Gross screening measures of cognitive function such as the Mini Mental State Examination may not be detailed or sensitive enough to detect cognitive changes associated with some risk factors.[19]

Genetic risk factors for dementia have been the subject of much research. The apolipoprotein E (APOE)-e4 allele, present in about 15% of whites, is a strong risk factor for AD.[21] APOE is a plasma protein involved in the metabolism of lipoproteins and plays a key role in the transport of cholesterol. The e4-allele may accelerate cognitive decline, particularly in the earliest stages of disease.[24]

Protective Factors. The protective factors (those that reduce the risk for cognitive decline) most consistently found in research are higher educational attainment, higher socioeconomic status, emotional support, better baseline cognitive function, better lung capacity, moderate alcohol use, and vitamin supplementation.[19] Some of the evidence on whether cognitive health can be improved by physical exercise is divided,[25] but studies with large sample sizes have found strong associations between physical activity and cognitive function.[26]

Treating vascular risk factors and maintaining vascular health are considered by some experts to be the keys to successful cognitive aging.[27] Table 1. lists preventive strategies that may improve vascular and cognitive health. Because so many of the protective factors for cardiovascular health and brain health are shared, what's good for the heart is probably also good for the brain.

Table 1. Strategies to Improve Vascular and Cognitive Health[27,28]

Preventive Strategy Possible Pathogenic Mechanisms/Positive Effects
Antihypertensive agents Hypertension may promote arteriosclerosis and occlude small vessels in the brain, causing chronic hypoperfusion of white matter and/or stroke. Hypertension may cause degenerative changes of intracerebral small vessels and compromise the blood-brain barrier.
Cholesterol-lowering agents Uncertain, although suppressing APOE secretion by statins could reduce the formation of cerebrovascular plaques and eventual neuronal death.
Antioxidants Reduction of free radicals may decrease oxidative injury to brain cells.
Vitamins (B12, folate) Low levels of vitamin B12 and folate are associated with cognitive symptoms.
Cholinesterase inhibitors Improved brain perfusion may preserve or slow the decline of regional reductions in brain blood flow.
Glycemic control Diabetes mellitus may lead to cognitive decline through ischemic cerebrovascular disease. Hyperglycemia may have direct toxic effect on neurons.
Antiplatelet treatment Uncertain, but may improve cerebral perfusion. Primary prevention of stroke may have a role in preventing vascular dementia.
Hormonal therapy Results are mixed. Hormone supplementation may protect against AD. Some evidence suggests that selective estrogen-receptor modulators may decrease the risk for mild cognitive impairment.
Smoking cessation Tobacco causes atherosclerosis, increasing the risk for silent brain infarctions. Increased oxidative stress may be toxic to neurons.
Diet Lower total fat, saturated fat, and cholesterol intake, and greater fish consumption (polyunsaturated fatty acids) may reduce the risk for cognitive decline.
Reducing stress Glucocorticoids can promote loss of hippocampal neurons. Increased oxidative stress and injury to the brain may occur as a result of increased production of oxidants and decreased production of antioxidant enzymes.
Exercise Regular exercise is associated with a reduced risk for cognitive impairment.
Social life An active social life involving networking, physical leisure, and other social activities, such as games, may reduce cognitive decline possibly because of a vascular effect or as a result of stress reduction.

AD = Alzheimer's disease; APOE = apolipoprotein E

An important protective factor for cognitive health is cognitive reserve.[29] Cognitive reserve refers to the hypothetical ability of the brain to compensate for age-associated degeneration, taking advantage of the brain's neuroplasticity by creating new neural pathways. Cognitive reserve may offer some resistance to the onset of clinical symptoms, allowing some individuals to cope with progressing AD pathology more effectively than others.[29] The degree of cognitive reserve in an individual may depend on factors such as innate intelligence, occupation, educational level, literacy, and a high level of participation in social and physical activities,[15,19] some of which may be proxies for innate or learned flexibility in responding to change.[10] In support of the cognitive reserve theory, research in animals and humans suggests that exposure to an enriched environment (physical activity, learning, social interaction) can influence the rate of neurogenesis in aging.[30]

Far fewer studies have explored variables that might encourage emotional health.[19] A comprehensive list of studies that investigated the variables that might predict cognitive and emotional health or decline can be found in the report of the Cognitive and Emotional Health Project.[31]


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