Cognitive decline

About: Cognitive decline is a research topic. Over the lifetime, 29308 publications have been published within this topic receiving 1174689 citations.

The mini-cog: a cognitive 'vital signs' measure for dementia screening in multi-lingual elderly.

Abstract: Objectives. The Mini-Cog, a composite of three-item recall and clock drawing, was developed as a brief test for discriminating demented from non-demented persons in a community sample of culturally, linguistically, and educationally heterogeneous older adults. Subjects. All 129 who met criteria for probable dementia based on informant interviews and 120 with no history of cognitive decline were included; 124 were non-English speakers. Methods. Sensitivity, specificity, and diagnostic value of the Mini-Cog were compared with those of the Mini-Mental State Exam (MMSE) and Cognitive Abilities Screening Instrument (CASI). Results. The Mini-Cog had the highest sensitivity (99%) and correctly classified the greatest percentage (96%) of subjects. Moreover, its diagnostic value was not influenced by education or language, while that of the CASI was adversely influenced by low education, and both education and language compromised the diagnostic value of the MMSE. Administration time for the Mini-Cog was 3 minutes vs 7 minutes for the MMSE. Conclusions. The Mini-Cog required minimal language interpretation and training to administer, and no test forms of scoring modifications were needed to compensate for the extensive linguistic and educational heterogeneity of the sample. Validation in clinical and population-based samples is warranted, as its brevity and ease of administration suggest that the Mini-Cog might be readily incorporated into general practice and senior care settings as a routine ‘cognitive vital signs’ measure. Copyright © 2000 John Wiley & Sons, Ltd.

Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline

Abstract: ContextAlzheimer disease (AD) is characterized neuropathologically by the presence of amyloid β-peptide (Aβ)–containing plaques and neurofibrillary tangles composed of abnormal tau protein. Considerable controversy exists as to whether the extent of accumulation of Aβ correlates with dementia and whether Aβ alterations precede or follow changes in tau.ObjectivesTo determine whether accumulation of Aβ correlates with the earliest signs of cognitive deterioration and to define the relationship between Aβ accumulation and early tau changes.Design, Setting, and PatientsPostmortem cross-sectional study of 79 nursing home residents with Clinical Dementia Rating (CDR) scale scores of 0.0 to 5.0 who died between 1986 and 1997, comparing the levels of Aβ variants in the cortices of the subjects with no (CDR score, 0.0 [n = 16]), questionable (CDR score, 0.5 [n = 11]), mild (CDR score, 1.0 [n = 22]), moderate (CDR score, 2.0 [n = 15]), or severe (CDR score, 4.0 or 5.0 [n = 15]) dementia.Main Outcome MeasuresLevels of total Aβ peptides with intact or truncated amino termini and ending in either amino acid 40 (Aβx-40) or 42 (Aβx-42) in 5 neocortical brain regions as well as levels of tau protein undergoing early conformational changes in frontal cortex, as a function of CDR score.ResultsThe levels of both Aβx-40 and Aβx-42 were elevated even in cases classified as having questionable dementia (CDR score = 0.5), and increases of both peptides correlated with progression of dementia. Levels of the more fibril-prone Aβx-42 peptide were higher than those of Aβx-40 in nondemented cases and remained higher throughout progression of disease in all regions examined. Finally, increases in Aβx-40 and Aβx-42 precede significant tau pathology at least in the frontal cortex, an area chosen for examination because of the absence of neuritic changes in the absence of disease.ConclusionsIn this study, levels of total Aβx-40 and Aβx-42 were elevated early in dementia and levels of both peptides were strongly correlated with cognitive decline. Of particular interest, in the frontal cortex, Aβ was elevated before the occurrence of significant tau pathology. These results support an important role for Aβ in mediating initial pathogenic events in AD dementia and suggest that treatment strategies targeting the formation, accumulation, or cytotoxic effects of Aβ should be pursued.

Handbook of the Biology of Aging

Abstract: Lower Organisms: Identification of Longevity. Assurance Genes in Yeast. Molecular Genetic Approaches to Identifying Gerontogenes in Caenorhabditis Elegans. Genetic Approaches to Life Prolongation in Drosophila Melonogaster. Mutants Affecting Senescence Processes in Plants. Changes in Gene Expression with Aging. Molecular and Cellular Biology: Mechanisms Controlling in Vitro Cellular Senescene. Mechanisms of Altered Gene Expression with Aging. Protein Modifications. Genomic and Mitochondrial DNA Alterations and Aging. Neurobiology: Neurobiological Correlates of Age-Related Cognitive Decline: Animal Models. Neuropyschological Assessment of Age-Related Cognitive Decline in Humans. Neuroendocrine Changes in Aging. Nerve Growth Factors, Neural Plasticity, And Aging. Human Biology: Aging Renal Function and Regulation of the Volume and Composition of the Extra Cellular Fluid. Depression in Old Age. Menopause and Its Consequences. Skeletal Integrity and Osteoporosis in Old Age. Overarching Areas: Excercisephysiology and Aging. Nutrition and Aging. Epidemiology of Aging.