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Commentary on “Comparison of clinical and neuropathologic diagnoses of Alzheimer's disease in 3 epidemiologic samples”
Author(s) -
Jellinger Kurt A.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.03.005
Subject(s) - citation , medical diagnosis , psychology , psychoanalysis , library science , medicine , psychiatry , gerontology , computer science , pathology
In their report on the validity of clinical diagnosis of Alzheimer’s disease (AD) using neuropathologic confirmation in 175 participants of 3 epidemiologic samples of demented individuals, Plassman et al [1] found a sensitivity of clinical diagnosis of probable or possible AD across the 3 studies of 92%. The rate of overall diagnostic agreement was 81%, not differing meaningfully across various levels of dementia severity. These findings can be confirmed largely by the data assessed in a sample of 207 elderly individuals from the Vienna Prospective Dementia study, performed between 1988 and 2001 in a geriatric hospital in Vienna, Austria [2]. It included 153 women and 54 men aged 58 to 102 years (mean 81.7 8.6 years), 200 with dementia, all fulfilling the clinical criteria according to International Classification of Diseases (ICD) 10 and Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, without clinical extrapyramidal (Parkinsonian) signs and symptoms, who underwent regular clinical, neuroimaging, and neuropsychological examination (including MiniMental-Score Examination [MMSE] and Clinical Dementia Rating [CDR] scores), the latter no longer than 6 months before death (mean 3.6 2.1 months). All patients underwent full postmortem evaluation and neuropathologic examination. The brains were examined according to an established protocol, and histologic examination was performed on multiple paraffin blocks of cerebral cortex, hippocampus, basal ganglia, and brainstem, using routine stains, modified Bielschowsky and Gallyas silver impregnation, and immunohistochemistry for tau-protein (antibody AT-8; Innogenetics, Ghent, Belgium), A amyloid peptide (clone 4G8; Signet Laboratories, Dedham, MA), GFAP (Daco, Gilstrup, Denmark), and alpha-synuclein (Chemicon, Hutheim, Germany). Postmortem diagnosis of AD followed the CERAD criteria [3], Braak staging of neuritic AD pathology [4], and the NIA-Reagan Institute criteria [5]. Diagnosis of other dementing disorders was made according to current guidelines for vascular dementia (VaD) and mixed dementia (AD plus vascular encephalopathy/MD) (see [6]), and dementia with Lewy bodies (DLB) [7], and others. The final clinical diagnosis was compared with neuropathologic diagnosis, and the final psychostatus using MMSE with Braak staging of neuritic AD pathology (see [8]).