Incidence Of Dementia In Patients Research Articles

The association between delirium and cognitive decline: a review of the empirical literature.

Delirium is a common neurobehavioral syndrome that occurs across health care settings which is associated with adverse outcomes, including death. There are limited data on long-term cognitive outcomes following delirium. This report reviews the literature regarding relationships between delirium and cognitive impairment. Psych Info and Medline searches and investigation of secondary references for all English language articles on delirium and subsequent cognitive impairment were carried out. Nine papers met inclusion criteria and documented cognitive impairment in patients following delirium. Four papers reported greater cognitive impairment among patients with delirium than matched controls. Four papers reported higher incidence of dementia in patients with a history of delirium. One study found 1 of 3 survivors of critical illness with delirium developed cognitive impairment. The evidence suggests a relationship between delirium and cognitive impairment, although significant questions remain regarding the nature of this association. Additional research on delirium-related effects on long-term cognitive outcome is needed.

A 10-year study of the incidence of and factors predicting dementia in Parkinson's disease.

To compare the incidence of dementia in PD with that of a control group without PD, and to assess the relationship between dementia and other features of PD. The authors recruited 83 patients with PD and 50 controls, all without dementia at initial assessment, and assessed them at regular intervals over a maximum period of 122 months. Dementia was diagnosed according to objective criteria, and included a judgment by researchers masked to subject group and to variables putatively associated with dementia. Seventeen patients fulfilled dementia criteria; no controls did so. The cumulative proportion of PD patients becoming demented by 112 months was 0.38 (95% CI 0.20 to 0.55), or 42.6 cases per 1000 years of observation. Univariate analyses showed that incident dementia in patients with PD was associated with older age at entry into the study, greater severity of neurologic symptoms, longer duration of PD, greater disability, and male sex. The association of age at onset of PD with incident dementia was of only borderline significance. Multivariate analysis found that age at entry into the study and severity of motor symptoms were significant predictors of dementia but duration of PD and age at onset of PD were not. Dementia in PD is likely to reflect interaction of the neuropathology of the basal ganglia and age-related pathology. The findings do not support the division of PD into early and late-onset cases.

Amyloid beta-peptide and the dementia of Parkinson's disease.

It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to "early" Alzheimer-type pathology. To determine whether amyloid beta-peptide (A beta) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for A beta. Twenty-three cases with PD had dementia, including all nine with A beta distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable A beta accumulation were not demented. Neither AD nor A beta deposition was increased in PD, furthermore, there was no statistical correlation between the amount of A beta and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to A beta, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or "early" Alzheimer-type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.

ALZ-50 staining of enteric neurons in Down syndrome in infants and children.

The monoclonal antibody ALZ-50, known to stain degenerating cerebral neurons in Alzheimer disease (AD), demonstrates a protein, A668, that is a modified form of the normal microtubule-associated protein, tau (1 -5). Because of the high incidence of an AD-like dementia in patients with Down syndrome (DS) who reach the age of 35-40 years (6-9), Wolozin et al. (10) studied ALZ-50 staining of temporal lobe neurons of 17 patients with DS aged from 16 fetal weeks to 62 years, finding ALZ-50 staining of these neurons in DS from ages 9 months to 6 years and from 29 to 62 years, whereas in control patients such staining was found from 34 to 36 fetal weeks to age 6 years but not in adults aged 28 to 91 years. These workers proposed that the protein demonstrable by ALZ-50 is developmentally regulated, with its expression reappearing during the third or fourth decade in patients with, but not in those without, DS. Although involvement of olfactory neurons in AD has been reported (1 1, 12), as has the occurrence in bowel wall of amyloid 0protein, a major component of the senile plaques found in the central neurons system in AD (13), we have found no reports on whether the neurons of the enteric nervous system show staining with ALZ-50 in DS or in non-DS infants and children. We have stained 5-pm sections from paraffin blocks of formalin-fixed tissues from various levels of the gastrointestinal tract of 13 DS patients, from 20 weeks of gestational age to 14 years, with biotinylated mouse monoclonal ALZ-50 antibody by a previously described avidin-biotin-horseradish peroxSupported in part by a grant from the Alzheimer Disease Consortium of the Universities of Southern

Dementia in Parkinson disease: a neuropathologic study.

Thirty-four autopsy cases conforming to the standard neuropathologic criteria of Parkinson disease were sex- and age-matched with controls who had died of infarct or trauma. All brains were reviewed for changes compatible with Alzheimer disease, and available clinical data were retrospectively reviewed. Nineteen (56 percent) of the Parkinson cases had shown some degree of dementia. The average parkinsonian brain weight was 1281 gm; it was 1365 gm for the controls (p less than 0.02). Plaques, neurofibrillary tangles, granulovacuolar degeneration, and cortical cell loss were present in all but one of the parkinsonian brains; these pathologic changes were present in fewer controls and to a lesser degree. The higher incidence of dementia in patients with Parkinson disease may be explained by the simultaneous presence of Alzheimer disease.