Achieving and Maintaining Cognitive Vitality With Aging
2002; Elsevier BV; Volume: 77; Issue: 7 Linguagem: Inglês
10.4065/77.7.681
ISSN1942-5546
AutoresHoward Fillit, Robert N. Butler, Alan W. O’Connell, Marilyn S. Albert, James E. Birren, Carl W. Cotman, William T. Greenough, Paul E. Gold, Arthur F. Kramer, Lewis H. Kuller, Thomas T. Perls, Barbara G. Sahagan, Tim Tully,
Tópico(s)Neuroinflammation and Neurodegeneration Mechanisms
ResumoCognitive vitality is essential to quality of life and survival in old age. With normal aging, cognitive changes such as slowed speed of processing are common, but there is substantial interindividual variability, and cognitive decline is clearly not inevitable. In this review, we focus on recent research investigating the association of various lifestyle factors and medical comorbidities with cognitive aging. Most of these factors are potentially modifiable or manageable, and some are protective. For example, animal and human studies suggest that lifelong learning, mental and physical exercise, continuing social engagement, stress reduction, and proper nutrition may be important factors in promoting cognitive vitality in aging. Manageable medical comorbidities, such as diabetes, hypertension, and hyperlipidemia, also contribute to cognitive decline in older persons. Other comorbidities such as smoking and excess alcohol intake may contribute to cognitive decline, and avoiding these activities may promote cognitive vitality in aging. Various therapeutics, including cognitive enhancers and protective agents such as antioxidants and anti-inflammatories, may eventually prove useful as adjuncts for the prevention and treatment of cognitive decline with aging. The data presented in this review should interest physicians who provide preventive care management to middle-aged and older individuals who seek to maintain cognitive vitality with aging. Cognitive vitality is essential to quality of life and survival in old age. With normal aging, cognitive changes such as slowed speed of processing are common, but there is substantial interindividual variability, and cognitive decline is clearly not inevitable. In this review, we focus on recent research investigating the association of various lifestyle factors and medical comorbidities with cognitive aging. Most of these factors are potentially modifiable or manageable, and some are protective. For example, animal and human studies suggest that lifelong learning, mental and physical exercise, continuing social engagement, stress reduction, and proper nutrition may be important factors in promoting cognitive vitality in aging. Manageable medical comorbidities, such as diabetes, hypertension, and hyperlipidemia, also contribute to cognitive decline in older persons. Other comorbidities such as smoking and excess alcohol intake may contribute to cognitive decline, and avoiding these activities may promote cognitive vitality in aging. Various therapeutics, including cognitive enhancers and protective agents such as antioxidants and anti-inflammatories, may eventually prove useful as adjuncts for the prevention and treatment of cognitive decline with aging. The data presented in this review should interest physicians who provide preventive care management to middle-aged and older individuals who seek to maintain cognitive vitality with aging. The "longevity revolution" has increased the focus on many aspects of health in aging. The older population is growing rapidly, and individuals are typically living longer, more active lives.1Rowe JW Kahn RL Successful Aging. Pantheon Books, New York, NY1998Google Scholar However, most older individuals still face late life with changes in cognitive function that affect quality of life2Committee on Future Directions for Cognitive Research on Aging Stern PC Carstensen LL The Aging Mind: Opportunities in Cognitive Research. National Academy Press, Washington, DC2000Google Scholar and increase mortality.3Bosworth HB Schaie KW Survival effects in cognitive function, cognitive style, and sociodemographic variables in the Seattle Longitudinal Study.Exp Aging Res. 1999; 25: 121-139Crossref PubMed Google Scholar Cognitive vitality in old age is impaired by both "normal cognitive aging" and diseases that cause dementia, primarily Alzheimer disease (AD) and vascular dementia. Although the cognitive impairments associated with normal aging have been defined and may impair quality of life,4Petersen RC Smith GE Waring SC Ivnik RJ Tangalos EG Kokmen E Mild cognitive impairment: clinical characterization and outcome [published correction appears in Arch Neurol. 1999;56:760].Arch Neurol. 1999; 56: 303-308Crossref PubMed Google Scholar, 5Crook T Bartus RT Ferris SH Whitehouse P Cohen GD Gershon S Age-associated memory impairment: proposed diagnostic criteria and measures of clinical change: report of a National Institute of Mental Health Work Group.Dev Neuropsychol. 1986; 2: 261-276Crossref Google Scholar, 6Schaie KW The course of adult intellectual development.Am Psychol. 1994; 49: 304-313Crossref PubMed Google Scholar, 7Schaie KW The hazards of cognitive aging.Gerontologist. 1989; 29: 484-493Crossref PubMed Google Scholar cognitive decline with aging is not inevitable, and many older adults, including some centenarians, appear to avoid cognitive decline even into the 11th decade of life.8Silver MH Jilinskaia E Perls TT Cognitive functional status of age-confirmed centenarians in a population-based study.J Gerontol B Psychol Sci Soc Sci. 2001; 56: P134-P140Crossref PubMed Google Scholar, 9Schaie KW Variability in cognitive function in the elderly: implications for societal participation.Basic Life Sci. 1988; 43: 191-211PubMed Google Scholar Recent research has resulted in new information identifying clinical risk factors for cognitive aging that are potentially modifiable. These new data support an emerging basis for primary and secondary prevention efforts to achieve and maintain cognitive vitality in late life. In this review, we discuss research that associates various risk factors with normal cognitive aging. Because most of these risk factors are potentially modifiable or manageable, such research should be of interest to physicians who provide preventive care counseling to older persons hoping to maintain cognitive vitality with aging. Cognitive decline, although a relatively common occurrence, cannot be considered an inevitable part of aging. Nature provides clear examples of elderly people who maintain cognitive vitality, even in extreme old age. Many older adults who live into their ninth decade retain high cognitive function,10Berkman LF Seeman TE Albert M et al.High, usual and impaired functioning in community-dwelling older men and women: findings from the MacArthur Foundation Research Network on Successful Aging.J Clin Epidemiol. 1993; 46: 1129-1140Abstract Full Text PDF PubMed Scopus (304) Google Scholar and centenarians who maintain their intellect negate the myth of the inevitability of cognitive decline.11Perls TT Morris JN Ooi WL Lipsitz LA The relationship between age, gender and cognitive performance in the very old: the effect of selective survival.J Am Geriatr Soc. 1993; 41: 1193-1201PubMed Google Scholar, 12Silver M Newell K Hyman B Growdon J Hedley-Whyte ET Perls T Unraveling the mystery of cognitive changes in old age: correlation of neuropsychological evaluation with neuropathological findings in the extreme old.Int Psychogeriatr. 1998; 10: 25-41Crossref PubMed Scopus (32) Google Scholar The aging brain remains capable of adapting to stimuli, and although declines in specific cognitive functions occur, some cognitive functions increase with age and can compensate for those functions that may decline. 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National Academy Press, Washington, DC2000Google Scholar Some cognitive functions, such as vocabulary, improve with age.16Birren JE Morrison DF Analysis of WAIS subtests in relation to age and education.J Gerontol. 1961; 16: 363-368Crossref PubMed Google Scholar Older people who are socially interactive and use additional information resources in solving everyday problems also show adaptivity.2Committee on Future Directions for Cognitive Research on Aging Stern PC Carstensen LL The Aging Mind: Opportunities in Cognitive Research. National Academy Press, Washington, DC2000Google Scholar Taken together, these findings suggest that individuals have varying degrees of "functional reserve" in their brains. Persons with high functional reserve may have increased capacity to keep learning and adapting despite age-related changes.17Baltes PB Baltes MM Psychological perspectives on successful aging: the model of selective optimization with compensation.in: Baltes PB Baltes MM Successful Aging: Perspectives From the Behavioral Sciences. Cambridge University Press, Cambridge, England1990: 1-34Crossref Google Scholar Increasing this functional reserve should promote cognitive vitality with aging. The underpinning of this functional reserve is likely to be brain plasticity, the ability of the brain to change structurally in response to stimuli. Recent neuroscience research shows that plasticity occurs via several mechanisms. 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Some processes required for maintaining normal neural function may become dysregulated with aging, causing neural damage.2Committee on Future Directions for Cognitive Research on Aging Stern PC Carstensen LL The Aging Mind: Opportunities in Cognitive Research. National Academy Press, Washington, DC2000Google Scholar Dysregulated inflammation (activation of microglia, cytokine release, and acute-phase response) may contribute to neuronal damage.37Mackenzie IR Munoz DG Nonsteroidal anti-inflammatory drug use and Alzheimer-type pathology in aging.Neurology. 1998; 50: 986-990Crossref PubMed Google Scholar, 38Selkoe DJ Translating cell biology into therapeutic advances in Alzheimer's disease.Nature. 1999; 399: A23-A31Crossref PubMed Google Scholar Oxidative stress, an imbalance between oxidative and antioxidant processes, may also cause neuronal damage in the aging brain.39Sayre LM Zagorski MG Surewicz WK Krafft GA Perry G Mechanisms of neurotoxicity associated with amyloid beta deposition and the role of free radicals in the pathogenesis of Alzheimer's disease: a critical appraisal.Chem Res Toxicol. 1997; 10: 518-526Crossref PubMed Scopus (92) Google Scholar, 40McDonald DR Brunden KR Landreth GE Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia.J Neurosci. 1997; 17: 2284-2294Crossref PubMed Google Scholar The pathologic changes associated with AD differ substantially from normal brain aging. 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From a clinical and an investigational perspective,3Bosworth HB Schaie KW Survival effects in cognitive function, cognitive style, and sociodemographic variables in the Seattle Longitudinal Study.Exp Aging Res. 1999; 25: 121-139Crossref PubMed Google Scholar types of cognitive decline with aging have been recognized: age-associated memory impairment (AAMI),5Crook T Bartus RT Ferris SH Whitehouse P Cohen GD Gershon S Age-associated memory impairment: proposed diagnostic criteria and measures of clinical change: report of a National Institute of Mental Health Work Group.Dev Neuropsychol. 1986; 2: 261-276Crossref Google Scholar mild cognitive impairment (MCI),4Petersen RC Smith GE Waring SC Ivnik RJ Tangalos EG Kokmen E Mild cognitive impairment: clinical characterization and outcome [published correction appears in Arch Neurol. 1999;56:760].Arch Neurol. 1999; 56: 303-308Crossref PubMed Google Scholar and dementia. 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People experiencing AAMI complain of memory loss but generally have normal scores on psychometric testing for their age group.5Crook T Bartus RT Ferris SH Whitehouse P Cohen GD Gershon S Age-associated memory impairment: proposed diagnostic criteria and measures of clinical change: report of a National Institute of Mental Health Work Group.Dev Neuropsychol. 1986; 2: 261-276Crossref Google Scholar This syndrome has been variously termed benign senescent forget- fulness and aging-related cognitive decline. For persons older than 50 years who complain of subjective memory loss, AAMI is defined as cognitive function that is 1 SD below the mean for young individuals on at least 1 psychometric memory test.5Crook T Bartus RT Ferris SH Whitehouse P Cohen GD Gershon S Age-associated memory impairment: proposed diagnostic criteria and measures of clinical change: report of a National Institute of Mental Health Work Group.Dev Neuropsychol. 1986; 2: 261-276Crossref Google Scholar, 54Sherwin BB Mild cognitive impairment: potential pharmacological treatment options.J Am Geriatr Soc. 2000; 48: 431-441PubMed Google Scholar Most data indicate that patients with AAMI do not progress to dementias such as AD. In addition, most data indicate that AAMI is not a prodromal state for MCI because less than 1% of people with AAMI will develop dementia. However, certainly some individuals with very early dementia may complain of mild memory loss akin to AAMI as their first symptom.55Bartres-Faz D Junque C Lopez-Alomar A et al.Neuropsychological and genetic differences between age-associated memory impairment and mild cognitive impairment entities.J Am Geriatr Soc. 2001; 49: 985-990Crossref PubMed Scopus (28) Google Scholar Nevertheless, more studies of rates of progression of AAMI to MCI or dementia are needed. Mild cognitive impairment describes older persons with subjective complaints of memory loss and objective psychometric measures of memory impairment compared with individuals of the same age.4Petersen RC Smith GE Waring SC Ivnik RJ Tangalos EG Kokmen E Mild cognitive impairment: clinical characterization and outcome [published correction appears in Arch Neurol. 1999;56:760].Arch Neurol. 1999; 56: 303-308Crossref PubMed Google Scholar However, these individuals do not have pronounced impairments in daily function and generally do not have impairment of other cognitive functions such as language or abstract thinking. Therefore, by definition, they do not have dementia. In a study of MCI, subjects performed 1.5 SDs below the mean for age- matched adults on memory tests, whereas other cognitive functions appeared relatively unaffected.4Petersen RC Smith GE Waring SC Ivnik RJ Tangalos EG Kokmen E Mild cognitive impairment: clinical characterization and outcome [published correction appears in Arch Neurol. 1999;56:760].Arch Neurol. 1999; 56: 303-308Crossref PubMed Google Scholar At least in some patients, MCI may be a prodromal syndrome of dementia. Up to 15% of individuals with MCI develop dementia each year, and 50% with MCI will develop dementia within 3 years of diagnosis. However, whether MCI is a separate entity or an early prodromal stage of dementia remains a matter of debate56Petersen RC Mild cognitive impairment or questionable dementia? 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Based on these studies, selected clinical interview questions may be useful to identify such converters, particularly questions related to delayed recall.58Daly E Zaitchik D Copeland M Schmahmann J Gunther J Albert M Predicting conversion to Alzheimer disease using standardized clinical information.Arch Neurol. 2000; 57: 675-680Crossref PubMed Google Scholar Dementia can be broadly defined as a syndrome of progressive global cognitive impairment severe enough to affect daily function.59Shumaker SA Reboussin BA Espeland MA et al.The Women's Health Initiative Memory Study (WHIMS): a trial of the effect of estrogen therapy in preventing and slowing the progression of dementia.Control Clin Trials. 1998; 19: 604-621Abstract Full Text Full Text PDF PubMed Scopus (129) Google Scholar The term dementia is reserved for chronic, progressive, irreversible, global cognitive impairment. Dementia is common in old age, with up to 25% of people older than 75 years and 40% of people older than 80 years having the illness.60Evans DA Funkenstein HH Albert MS et al.Prevalence of Alzheimer's disease in a community population of older persons: higher than previously reported.JAMA. 1989; 262: 2551-2556Crossref PubMed Google Scholar The most common causes are clearly AD and vascular dementia. Other causes of dementia include Parkinson disease, Lewy body disease, and other more rare neurodegenerative conditions.61Paist III, SS Martin JR Brain failure in older patients: uncovering treatable causes of a diminished ability to think.Postgrad Med. May 1996; 99 (130-134, 136.): 125-128PubMed Google Scholar, 62Rockwood K Bowler J Erkinjuntti T Hachinski V Wallin A Subtypes of vascular dementia.Alzheimer Dis Assoc Disord. 1999; 13: S59-S65PubMed Google Scholar As discussed previously, at present there is no known neuro- pathogenic relationship between cognitive aging and AD. Alzheimer disease is not considered an accelerated form of cognitive aging, but rather a disease primarily of old persons. Emerging research has resulted in a growing understanding of the potentially modifiable risk factors associated with cognitive decline in late life, and several interventions are being evaluated in research studies to prevent cognitive decline and dementia in older persons (Table 1).63Fillit HM Butler RN Cognitive Decline: Strategies for Prevention. Greenwich Medical Media, London, England1997Google ScholarTable 1Possible Strategies to Promote Cognitive Vitality With Aging Early detection of individuals at risk Neuropsychological testingNeuroimagingBiomarkersGenetic markersLifestyle management Build "cognitive reserve" by remaining intellectually and socially active Continue life
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