Prevalence of cognitive impairment

Unverzagt, Frederick W.; Gao, Sujuan; Baiyewu, Olusegun; Ogunniyi, Adesola; Gureje, Oye; Perkins, Anthony J.; Emsley, Christine L.; Dickens, J.; Evans, Rebecca M.; Musick, Beverly; Hall, Kathleen; Hui, Siu L.; Hendrie, Hugh C.

doi:10.1212/wnl.57.9.1655

Cited by 276 publications

(217 citation statements)

References 28 publications

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“…This group is likely to be heterogeneous, including persons with non-AD forms of memory impairment as well as persons who are transiently cognitively impaired (Unverzagt et al, 2001). Such heterogeneity would undermine the assumption of medial temporal lobe pathology in the memory-impaired participants and make it less likely we would find the hypothesized pattern of effects.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies suggest that there may be a large reservoir of mildly cognitively impaired persons in the community (DiCarlo et al, 2000;Ganguli et al, 2004a;Graham et al, 1997;Lopez et al, 2003;Unverzagt et al, 2001). A major cause of abnormal cognitive aging is Alzheimer disease (AD) which, in its initial stages, is characterized clinically by impairment in declarative memory and neuropathologically by intracellular deposits of tau, in the form of neurofibrillary tangles, extracellular deposits of beta-amyloid, and neuronal loss in the medial temporal lobe including the hippocampus and entorhinal cortex.…”

Section: Introductionmentioning

confidence: 99%

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Effect of memory impairment on training outcomes in ACTIVE

Unverzagt

Kasten

Johnson

et al. 2007

J Int Neuropsychol Soc

107

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Cognitive training improves mental abilities in older adults, but the trainability of persons with memory impairment is unclear. We conducted a subgroup analysis of subjects in the Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) trial to examine this issue. ACTIVE enrolled 2802 non-demented, community-dwelling adults aged 65 years and older and randomly assigned them to one of four groups: Memory training, reasoning training, speed-of-processing training, or no-contact control. For this study, participants were defined as memory-impaired if baseline Rey Auditory Verbal Learning Test (AVLT) sum recall score was 1.5 SD or more below predicted AVLT sum recall score from a regression-derived formula using age, education, ethnicity, and vocabulary from all subjects at baseline. Assessments were taken at baseline (BL), post-test, first annual (A1), and second annual (A2) follow-up. One hundred and ninety-three subjects were defined as memory-impaired and 2580 were memory-normal. Training gain as a function memory status (impaired vs. normal) was compared in a mixed effects model. Results indicated that memoryimpaired participants failed to benefit from Memory training but did show normal training gains after reasoning and speed training. Memory function appears to mediate response to structured cognitive interventions in older adults.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of memory impairment on training outcomes in ACTIVE

Unverzagt

Kasten

Johnson

et al. 2007

J Int Neuropsychol Soc

107

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“…T wenty-five percent of individuals over 65 years of age have sufficient cognitive problems, short of dementia, to affect the quality of their lives (1,2). The ability to learn consciously and recall new information, which is known as recent or declarative memory, is one of the areas most affected during aging.…”

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confidence: 99%

“…In addition, nondiabetic individuals with mild forms of impaired glucose tolerance (IGT) may also have cognitive impairments (7,8). The prevalence of memory problems and IGT rise with age (1,9,10). In addition to genetic predisposition, obesity and low levels of physical activity have been identified as risk factors for IGT in adults and children (11,12).…”

mentioning

confidence: 99%

Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly

Convit

Wolf²,

Tarshish³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

293

181

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Poor glucose tolerance and memory deficits, short of dementia, often accompanies aging. The purpose of this study was to ascertain whether, among nondiabetic, nondemented middle-aged and elderly individuals, poorer glucose tolerance is associated with reductions in memory performance and smaller hippocampal volumes. We studied 30 subjects who were evaluated consecutively in an outpatient research setting. The composition of the participant group was 57% female and 68.6 ؎ 7.5 years of age; the participants had an average education of 16.2 ؎ 2.3 years, a score on the Mini Mental State Examination of 28.6 ؎ 1.5, a glycosylated hemoglobin (HbA1C) of 5.88 ؎ 0.74%, and a body mass index of 24.9 ؎ 4.1 kg͞m 2 . Glucose tolerance was measured by an i.v. glucose tolerance test. Memory was tested by using the Wechsler Paragraphs recall tests at the time of administering the i.v. glucose tolerance test. The hippocampus and other brain volumes were measured by using validated methods on standardized MRIs. Decreased peripheral glucose regulation was associated with decreased general cognitive performance, memory impairments, and atrophy of the hippocampus, a brain area that is key for learning and memory. These associations were independent of age and Mini Mental State Examination scores. Therefore, these data suggest that metabolic substrate delivery may influence hippocampal structure and function. This observation may bring to light a mechanism for aging brain injury that may have substantial medical impact, given the large number of elderly individuals with impaired glucose metabolism.T wenty-five percent of individuals over 65 years of age have sufficient cognitive problems, short of dementia, to affect the quality of their lives (1, 2). The ability to learn consciously and recall new information, which is known as recent or declarative memory, is one of the areas most affected during aging. However, our knowledge about the medical factors that predispose a person to age-associated cognitive problems remains undeveloped.There is a growing literature indicating that individuals with diabetes have impairments in recent memory (3-6). In addition, nondiabetic individuals with mild forms of impaired glucose tolerance (IGT) may also have cognitive impairments (7,8). The prevalence of memory problems and IGT rise with age (1, 9, 10). In addition to genetic predisposition, obesity and low levels of physical activity have been identified as risk factors for IGT in adults and children (11,12). With life expectancy and obesity on the rise, the prevalence of memory dysfunction and IGT will likely continue to climb. However, it remains to be established whether there are associations between peripheral glucose regulation and memory performance among nondemented middleaged and elderly individuals.The hippocampus, a brain structure deep in the temporal lobe, is key for recent memory formation (13-15). Hypothalamuspituitary-adrenal axis hyperactivity have been associated with hippocampal atrophy in aging (16) and in Cushing's disease (1...

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“…Epidemiological data from different countries have shown a prevalence rate of MCI in the range of 14% to 18% for individuals aged 70 years and older (Busse et al, 2006;Das et al, 2007;Di Carlo et al, 2007;Fischer et al, 2007;Ganguli Dodge, Shen, & DeKosky, 2004;Hänninen et al, 2002;Lopez et al, 2003;Manly et al, 2008;Palmer, Bäckman, Winglad, & Fratiglioni, 2008;Plassman et al, 2008;Petersen et al, 2009;Roberts et al, 2008;Unverzagt et al, 2001). Despite variations, the overall estimated incidence rates of nonspecific MCI have been in the range of 51 to 76.8 cases per 1,000 person-years.…”

Section: Mild Cognitive Impairmentmentioning

confidence: 99%

Neuropsychological and neurobiological markers of the preclinical stage of Alzheimer’s disease.

Fichman

Oliveira

Fernandes

2011

Psychology & Neuroscience

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Dementia, especially Alzheimer's disease, has a high prevalence in the elderly population. Therefore, identifying individuals who are at a high risk for early diagnosis is crucial to allow both pharmacological and behavioral therapeutic interventions, which in some cases can delay the progression of dementia. This paper describes neuropsychological and neurobiological markers for the early diagnosis of Alzheimer's disease and presents the main risk factors, including neuropathological, neuroanatomical, neurofunctional, genetic, and neuropsychological. The literature shows that the combination of these markers is the best method for predicting Alzheimer's disease, years before its clinical manifestation. The most prevalent neurobiological and neuropsychological risk factors include (1) senile plaques and neurofibrillary tangles in the medial temporal lobe and cortical regions, (2) low concentrations of Aβ1-42 peptide and high concentrations of total tau protein and phosphorylated tau protein in cerebrospinal fluid, (3) reduced global cerebral volume, increased ventricular volume, and atrophy in the hippocampal formation and entorhinal cortex, (4) global reductions in cerebral metabolism and perfusion in the temporoparietal junction, temporal, parietal, and frontal lobes, hippocampal formation, and posterior cingulate cortex, (5) the presence of the apolipoprotein E ε4 allele, and (6) verbal anterograde episodic long-term memory impairment and executive dysfunction. The present review discusses the evidence for markers that identify individuals who are at a high risk of developing Alzheimer's disease and the importance of longitudinal studies in this context.

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Prevalence of cognitive impairment

Abstract: Cognitive impairment short of dementia affects nearly one in four community-dwelling elders and is a major risk factor for later development of dementia.

Cited by 276 publications

References 28 publications

Effect of memory impairment on training outcomes in ACTIVE

Effect of memory impairment on training outcomes in ACTIVE

Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly

Neuropsychological and neurobiological markers of the preclinical stage of Alzheimer’s disease.

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