1c:I[419806,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/30036bedc5269936.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/cd5e572bc3e4eb92.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/d4ac9dcf27f6ff52.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 1d:T44e,Diagnostic Criteria From DSM-IV,by the American Psychiatric Association, 358 pp, spiral-bound, $22.50, ISBN 0-89042-064-5, Washington, DC, American Psychiatric Press Inc, 1994. DSM-IV Sourcebook, vol 1, edited by Thomas A. Widiger, Allen J. Frances, Harold Alan Pincus, Michael B. First, Ruth Ross, and Wendy Davis, 768 pp, $112.50, ISBN 0-89042-065-3, Washington, DC, American Psychiatric Association, 1994. DSM-IV: Diagnostic and Statistical Manual of Mental Disorders, fourth edition, was developed with a great deal of input from mental health professionals and professional organizations. In addition, there was a significant collaboration between the American Psychiatric Association (APA) and the World Health Organization, as it developed the tenth revision of theInternational Statistical Classification of Diseases and Related Health Problems (ICD-10). As a result, DSM-IV is a great improvement over the third edition(DSM-III)and the third edition, revised(DSM-III-R). The Task Force onDSM-IVand 13 work groups (each responsible for a section1e:T528,Hyperphosphorylated tau protein (P-tau) in CSF is a core biomarker candidate of Alzheimer's disease. Hyperphosphorylation of tau is thought to lead to neurofibrillary changes, a neuropathological hallmark of this type of dementia. Currently, the question is unresolved whether CSF levels of P-tau reflect neurofibrillary changes within the brain of a patient with the illness. Twenty-six patients were included with intra-vitam CSF as well as post-mortem neuropathological data. In the CSF, P-tau phosphorylated at threonine 231 (P-tau231P) was analysed. Post-mortem, scores of neurofibrillary tangles (NFT) and neuritic plaques (NP) were assessed in frontal, temporal, parietal and hippocampal cortical areas. In the same cortical regions, load of hyperphosphorylated tau protein (HP-tau load) was determined. Concentrations of P-tau231P were measured in frontal cortex homogenates. We found significant correlations between CSF P-tau231P concentrations and scores of NFTs and HP-tau load in all neocortical regions studied. The score of NPs was correlated with CSF P-tau231P only within the frontal cortex. There was a correlation between P-tau231P in CSF and brain homogenates. These findings indicate that CSF P-tau231P may serve as an in vivo surrogate biomarker of neurofibrillary pathology in Alzheimer's disease.

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