
Am J Psychiatry 160:867-872, May 2003
© 2003 American Psychiatric Association
Amyloid ß Pathology in Alzheimers Disease and Schizophrenia
Dorota Religa, M.D.,
Hanna Laudon, M.Sc.,
Maria Styczynska, M.D.,
Bengt Winblad, M.D., Ph.D.,
Jan Näslund, Ph.D., and
Vahram Haroutunian, Ph.D.
OBJECTIVE: Severe cognitive impairment is common in elderly patients with schizophrenia. Alzheimers disease is the main cause of dementia among the elderly. Biochemical and genetic studies suggest that amyloid ß-peptide is central in Alzheimers disease. The authors examined the possible involvement of amyloid ß-peptide in cognitive impairment in schizophrenia. METHOD: Specific antibodies against two major forms of amyloid ß-peptide, Aßx-40 and Aßx-42, were used in sandwich enzyme-linked immunosorbent assays to determine the levels of amyloid ß-peptide in postmortem brain samples from Alzheimers disease patients (N=10), normal elderly comparison subjects (N=11), and schizophrenia patients with (N=7) or without (N=26) Alzheimers disease. RESULTS: The levels of amyloid ß-peptide were highest in the Alzheimers disease patients, followed by the patients with schizophrenia and comparison subjects. The mean Aßx-42 level in the schizophrenia patients without Alzheimers disease was similar to that in the comparison subjects, but the level in the schizophrenia patients with Alzheimers disease was significantly higher than in those without Alzheimers disease or the comparison subjects. The Aßx-42 level in the schizophrenia patients with Alzheimers disease was significantly lower than the level in the Alzheimers disease cohort. CONCLUSIONS: In contrast to elderly schizophrenia patients with Alzheimers disease pathology, those without Alzheimers disease had amyloid ß-peptide levels that were not significantly different from those of normal subjects; hence amyloid ß-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 Alzheimers disease.
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D. Religa, D. Strozyk, R. A. Cherny, I. Volitakis, V. Haroutunian, B. Winblad, J. Naslund, and A. I. Bush
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