The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Amyloid beta pathology in Alzheimer's disease and schizophrenia.
Dorota Religa; Hanna Laudon; Maria Styczynska; Bengt Winblad; Jan Näslund; Vahram Haroutunian (Profiled Author: Winblad, Bengt)
Department of Clinical Neuroscience, Occupational Therapy and Elderly Care Research, Karolinska Institutet, 141 86 Huddinge, Sweden. firstname.lastname@example.org
The American journal of psychiatry 2003;160(5):867-72.
OBJECTIVE: Severe cognitive impairment is common in elderly patients with schizophrenia. Alzheimer's disease is the main cause of dementia among the elderly. Biochemical and genetic studies suggest that amyloid beta-peptide is central in Alzheimer's disease. The authors examined the possible involvement of amyloid beta-peptide in cognitive impairment in schizophrenia. METHOD: Specific antibodies against two major forms of amyloid beta-peptide, Abetax-40 and Abetax-42, were used in sandwich enzyme-linked immunosorbent assays to determine the levels of amyloid beta-peptide in postmortem brain samples from Alzheimer's disease patients (N=10), normal elderly comparison subjects (N=11), and schizophrenia patients with (N=7) or without (N=26) Alzheimer's disease. RESULTS: The levels of amyloid beta-peptide were highest in the Alzheimer's disease patients, followed by the patients with schizophrenia and comparison subjects. The mean Abetax-42 level in the schizophrenia patients without Alzheimer's disease was similar to that in the comparison subjects, but the level in the schizophrenia patients with Alzheimer's disease was significantly higher than in those without Alzheimer's disease or the comparison subjects. The Abetax-42 level in the schizophrenia patients with Alzheimer's disease was significantly lower than the level in the Alzheimer's disease cohort. CONCLUSIONS: In contrast to elderly schizophrenia patients with Alzheimer's disease pathology, those without Alzheimer's disease had amyloid beta-peptide levels that were not significantly different from those of normal subjects; hence amyloid beta-peptide does not account for the cognitive deficits in this group. These results suggest that the causes of cognitive impairment in "pure" schizophrenia are different from those in Alzheimer's disease.
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