Learning and Longevity

Learning has emerged as a factor in prolonging life and reducing disability and disease in old age (Box 2). Epidemiologic studies have reported that there is a positive correspondence between life expectancy and amount of schooling one receives (95,96). The benefit of education persists when "active" life expectancy or life free of disabilities is compared to "total" life expectancy or life with disabilities and this finding is irrespective of sex and race. As Katzman (97) quotes, "Scholars grow wiser with age, but the noneducated become foolish." A higher level of education seems also to be associated with a lower prevalence of AD (98). In a long-term investigation, started in l986 and continuing today (the "Nun Study"), 678 Catholic nuns are being studied for the relationship between their writing proficiency at a young age and continuing in middle and old age, and their longevity and incidence of dementia (99). Reports to date indicate that those with the higher writing proficiency at a young age lived longer and had a lower incidence of AD (99,100).

According to one Japanese proverb: "Aging starts when we stop learning." Learning may be defined as the ability of the individual to alter behavior on the basis of experience. Learning depends, in part, on memory, which may be defined, in a large context, as a reception-processing-storage-retrieval function of the brain and the mind. It is the ability to recall past events. While "learning" and "memory" are integral to each other, both come in different forms that are thought to depend on different neural mechanisms and sites in the nervous system. It is not surprising then that changes in different kinds of learning and memory do not necessarily parallel each other. Environmental

FIGURE 4 PET scans taken with the glucose metabolic tracer FDG. In these scans, whiter colors represent higher glucose metabolism. Two individuals, one with AD and one normal older person were studied, and each of four images represents a brain "slice" from the top of the head to the bottom (rostral to caudal). The AD patient shows reduced glucose metabolism in the parietal-temporal cortex, illustrated with white arrows. Also visible on these scans are the ventricles (black arrow, upper left image) and basal ganglia (black arrow, upper right image), which can be clearly seen in both subjects. Ventricular enlargement may be seen more clearly on MRI scans. Basal ganglia glucose metabolism is relatively preserved in AD. Abbreviations: PET positron emission tomography; FDG, [18F]fluorodeoxyglucose; AD, Alzheimer's disease; MRI, magnetic resonance imaging. Source: Courtesy of Dr. W.J. Jagust.

FIGURE 4 PET scans taken with the glucose metabolic tracer FDG. In these scans, whiter colors represent higher glucose metabolism. Two individuals, one with AD and one normal older person were studied, and each of four images represents a brain "slice" from the top of the head to the bottom (rostral to caudal). The AD patient shows reduced glucose metabolism in the parietal-temporal cortex, illustrated with white arrows. Also visible on these scans are the ventricles (black arrow, upper left image) and basal ganglia (black arrow, upper right image), which can be clearly seen in both subjects. Ventricular enlargement may be seen more clearly on MRI scans. Basal ganglia glucose metabolism is relatively preserved in AD. Abbreviations: PET positron emission tomography; FDG, [18F]fluorodeoxyglucose; AD, Alzheimer's disease; MRI, magnetic resonance imaging. Source: Courtesy of Dr. W.J. Jagust.

BOX 2 Continuing Education Throughout the Life Span

The beneficial effects of education in prolonging life span and postponing the onset of disability and disease, although intellectually appealing, are in need of continuing experimental and clinical support. As private research and government health programs attempt to improve our understanding of biologic phenomena, so must all organizations devoted to improving quality-of-life at all ages recognize the value of continuing education to human health. By establishing a robust brain reserve at young ages, it is possible to draw from this reserve as we grow old and/or become disabled or ill. Given our present knowledge that the plasticity of the nervous system persists even in old age, the outlook for at least some degree of regeneration and compensation is brighter than it once was. Combined with other biologic and psychologic evidence, there is every reason to support education as an important tool in the eternal quest for a better and longer life.

changes trigger sensory responses that, in turn, modify the nervous system so that animals can learn and remember. This learning and remembering ability, which can be viewed as an expression of neural plasticity (Chapter 6) is altered with aging, despite the persistence of compensatory adjustments even in old individuals (Fig. 3) (101).

The beneficial effects of education on longevity and, indirectly, on normal and abnormal aging, has been ascribed to a number of factors, the most obvious being a better socioeconomic status (e.g., higher family income and greater employment opportunities) (Table 6) (Box 2). One of the most challenging interpretations of these observations is that extended learning may prevent (or at least, delay) the aging-related losses that occur in the nervous system with old age (102,103). The active process of learning is thought to build up a "brain reserve" in the form of an increased number and enhanced function of neurons and glial cells, better cerebral blood flow, higher oxygen levels, and glucose metabolism. Such an increased brain reserve may manifest itself as

■ reduced or delayed neuronal losses or, conversely,

■ reestablishment of neuronal and glial proliferation,

■ increased synaptic density,

■ changes in neurotransmitter levels (e.g., reduced sensitivity to excitotoxins),

■ changes in receptor number and sensitivity (e.g., NGF low-or high-affinity receptors stimulate or inhibit apoptosis, respectively), and

During normal brain aging as well as in the presence of disease, degenerative processes are often associated with adaptive growth and regeneration (101-103). Continued learning may act by inducing and strengthening these adaptive responses at all ages, including old age, thereby giving validity to the well-known adage "use it or lose it" (Box 2) (103).

TABLE 6 Mechanisms of the Effects of Increased Education on Successful Aging

Adequate income

Better access to medical care Better access to recreational activity Good nutrition

Responsible health behaviors Moderate alcohol intake Abstinence from smoking Possibility of increased brain reserve capacity More dendritic branching, more synapses Better cerebral blood flow

Better neural cell efficiency, adaptability, survival, and growth

■ SENILE DEMENTIAS

■ Definitions and Prevalence

Dementia (from the Latin 'de-mens', without mind) is a clinical syndrome that refers to a global deterioration of intellectual and cognitive functions characterized by a decline of all five major mental functions—orientation, memory, intellect, judgment, and affect—but with persistence of a clear consciousness. Dementia caused by a variety of factors may occur at all ages and may be reversible or irreversible. The concept of a reversible dementia is sometimes a confusing one and needs to be accurately described, especially when dealing with individual elderly patients and their caregivers.

Reversible dementia is a subacute condition of impaired cognition to be contrasted to reversible acute changes in cognition, defined as delirium (the two concepts may be semantically confused). It is generally due to known causes, and once these are removed (e.g., drugs) or treated (e.g., infections), the dementia may be ameliorated. A handy mnemonic to remember the main causes of reversible dementia is presented in Table 7. A list of types of cognitive impairment in the elderly, to be differentiated from dementia, is presented in Table 8. Among these types, delirium is particularly alarming in the demented elderly, since the condition is associated with high morbidity and mortality (104).

In the elderly, dementia may occur due to multiple, but still little known factors. In most cases, dementia is irreversible and progressive (i.e., worsens with time). According to causes, pathology, and clinical manifestations, dementia has been categorized in several types, the distribution of which is illustrated in Figure 5:

■ Dementia of AD accounts for 50% to 60% of all senile dementia cases.

■ Vasomotor dementias and Lewy-body dementia account for 20% to 30% of all cases.

■ Reversible dementias, as listed in Table 7, account for 10% to 20% of all cases.

TABLE 7 Underlying and Reversible Causes of Dementia

D Drugs

E Emotional disorders

M Mfetabolic or endocrine disorders

E Eye and ear dysfunctions

N Nutritional deficiencies

T Tumor and trauma

I /nfections

A Atheriosclerotic complications, i.e., myocardial infarction, stroke, or heart failure

TABLE 8 Types of Cognitive Impairment in the Elderly To Be Differentiated from AD

Delirium: An acute alteration of mental status characterized by inattention and disordered thinking. Other symptoms include clouding of consciousness and fluctuation of symptoms. Severity ranges from mild to severe. Delirium is reversible, with improvement of mental function occurring after the underlying medical condition has been treated. Delirium is particularly problematic in the elderly, especially those who are already demented, inasmuch as it is responsible for high morbidity and mortality (104) Depression: A specific psychiatric entity that can precede or be associated with dementia and that can be differentially diagnosed and treated

AAMI: Normal aging changes, not progressive and not of sufficient severity to interfere with daily function. Mild cognitive impairment is an entity describing those in the nonspecific interface area between AAMI and early AD (69) Paranoid states and psychoses: Patients presenting with specific diagnostic psychiatric correlates Amnesic syndrome: Characterized by inability to register new information but without delirium or dementia

Abbreviations: AAMI, age-associated memory impairment; AD, Alzheimer's disease.

■ Depression or pseudodementias (i.e., condition in which symptoms of depression may mimic or mask those of dementia) (105) account for 1% to 5% of all cases.

■ The remainder comprise miscellaneous disorders such as Parkinson's disease, and Pick's disease (see below).

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