A new rating scale for Alzheimer's disease Am J Psychiatry 141: 1356-1364

American Journal of Psychiatry (Impact Factor: 12.3). 12/1984; 141(11):1356-64. DOI: 10.1176/ajp.141.11.1356
Source: PubMed


A new rating instrument, the Alzheimer's Disease Assessment Scale, was designed specifically to evaluate the severity of cognitive and noncognitive behavioral dysfunctions characteristic of persons with Alzheimer's disease. Item descriptions, administration procedures, and scoring are outlined. Twenty-seven subjects with Alzheimer's disease and 28 normal elderly subjects were rated on 40 items. Twenty-one items with significant intraclass correlation coefficients for interrater reliability (range, .650-.989) and significant Spearman rank-order correlation coefficients for test-retest reliability (range, .514-1) constitute the final scale. Subjects with Alzheimer's disease had significantly more cognitive and noncognitive dysfunction than the normal elderly subjects.

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Available from: Richard C Mohs, Aug 20, 2014
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    • "Efficacy measures were collected at baseline assessment and after 1, 3, 6, 12, 18, 24, and 36 months. The following variables were collected by blinded raters (psychologists): – Cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog) [18]. This was the primary efficacy measure. "
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    ABSTRACT: Background: Little is known about the long-term acceptance and effects of cognitive and motor stimulation interventions (CMSI) in Alzheimer's disease (AD). Objective: To evaluate a replicable CMSI program for mild cognitive impairment (MCI) and mild-to-moderate AD persons. Methods: Eighty-four non-institutionalized subjects with AD were randomized to receive either CMSI, administered by a single care provider, or standard support. Cognition, activities of daily living (ADL), mood, and study partner's subjective burden were assessed by blinded raters. Data on institutionalization, psychiatric medications, and demise were collected by the study physicians. Random effects model and survival analyses were conducted, after 2 and 3 years of study. Results: Three-year assessments could be performed by the physician in 85% and by the blinded rater in 66% of subjects. Significant benefits were observed in basic ADL at the 2- and 3-year assessments, whereas instrumental ADL showed benefits only up to the second year of intervention (p < 0.05). Conclusion: Long-term cognitive-motor stimulation is well accepted and produces functional benefits in subjects with AD, with no extra subjective burden in the partner.
    Journal of Alzheimer's disease: JAD 12/2014; 45(1). DOI:10.3233/JAD-142364 · 4.15 Impact Factor
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    • "As outcome measures we used 6 endophenotype markers of AD. Two markers were tests of cognition: MMSE and Alzheimer's Disease Assessment Scale Cognition (ADAS) for ADNI and DCN or MMSE and CAMCOG for ADC (Derix et al., 1991; Folstein et al., 1975; Rosen et al., 1984). Three markers were CSF biomarkers of AD: abeta, tau, and ptau. "
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    ABSTRACT: We studied the association of SORL1 single-nucleotide polymorphisms genotypes with measures of pathology in patients with probable Alzheimer's disease (AD) using an endophenotype approach. We included (1) 133 patients from the German Dementia Competence Network (71 ± 8 years; 50% females; Mini Mental State Examination [MMSE], 24 ± 3); (2) 83 patients from the Alzheimer's Disease Neuroimaging Initiative (75 ± 8 years; 45% females; MMSE, 24 ± 2); and (3) 452 patients from the Amsterdam Dementia Cohort 66 ± 8 years; 47% females; MMSE, 20 ± 5). As endophenotype markers we used cognitive tests, cerebrospinal fluid (CSF) biomarkers amyloid-beta, total tau (tau), tau phosphorylated at threonine 181, and hippocampal atrophy. We measured 19 SORL1 SNP alleles. Genotype-endophenotype associations were determined by linear regression analyses. There was an association between rs2070045-G allele and increased CSF-tau and more hippocampal atrophy. Additionally, haplotype-based analyses revealed an association between haplotype rs11218340-A/rs3824966-G/rs3824968-A and higher CSF-tau and CSF-tau phosphorylated at threonine 181. In conclusion, we found that SORL1 SNP rs2070045-G allele was related to CSF-tau and hippocampal atrophy, 2 endophenotype markers of AD, suggesting that SORL1 may be implicated in the downstream pathology in AD. Copyright © 2015 Elsevier Inc. All rights reserved.
    Neurobiology of Aging 12/2014; 36(3). DOI:10.1016/j.neurobiolaging.2014.12.007 · 5.01 Impact Factor
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    • "Informed consent was obtained from either the patient or a surrogate after the nature and possible consequences of DBS surgery were explained. Patient demographics, medication use, and baseline and one-year Alzheimer's Disease Assessment Scale-Cognitive Subscale-11 (ADAS-Cog) [19] scores are reported in Table 1. Additional neuropsychological data included: MMSE, verbal fluency as measured using animal fluency, intelligence quotient (IQ) measured using the Wechsler Abbreviated Scale of Intelligence [20], trail making test A and B [21], and face recognition using the Wechsler Memory Scale, 3rd edition [22] (Supplementary Tables 1 and 2). "
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    ABSTRACT: Deep Brain Stimulation (DBS) is thought to improve the symptoms of selected neurological disorders by modulating activity within dysfunctional brain circuits. To date, there is no evidence that DBS counteracts progressive neurodegeneration in any particular disorder. We hypothesized that DBS applied to the fornix in patients with Alzheimer's Disease (AD) could have an effect on brain structure. In six AD patients receiving fornix DBS, we used structural MRI to assess one-year change in hippocampal, fornix, and mammillary body volume. We also used deformation-based morphometry to identify whole-brain structural changes. We correlated volumetric changes to hippocampal glucose metabolism. We also compared volumetric changes to those in an age-, sex-, and severity-matched group of AD patients (n = 25) not receiving DBS. We observed bilateral hippocampal volume increases in the two patients with the best clinical response to fornix DBS. In one patient, hippocampal volume was preserved three years after diagnosis. Overall, mean hippocampal atrophy was significantly slower in the DBS group compared to the matched AD group, and no matched AD patients demonstrated bilateral hippocampal enlargement. Across DBS patients, hippocampal volume change correlated strongly with hippocampal metabolism and with volume change in the fornix and mammillary bodies, suggesting a circuit-wide effect of stimulation. Deformation-based morphometry in DBS patients revealed local volume expansions in several regions typically atrophied in AD. We present the first in-human evidence that, in addition to modulating neural circuit activity, DBS may influence the natural course of brain atrophy in a neurodegenerative disease. Copyright © 2015 Elsevier Inc. All rights reserved.
    Brain Stimulation 12/2014; 8(3). DOI:10.1016/j.brs.2014.11.020 · 4.40 Impact Factor
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