A dose-ranging study of lecithin in the treatment of primary degenerative dementia (Alzheimer disease).
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Biomedical subjects
Publications and source records attributed to N Pomara.
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Complement activation is present in the brain in Alzheimer's disease (AD), and C1q concentrations are decreased in AD cerebrospinal fluid (CSF). To determine whether concentrations of other complement proteins are also altered in AD CSF, we measured concentrations of C3a and SC5b-9 in CSF from patients with probable AD (n = 19), normal aged controls (n = 11), and normal younger controls (n = 15). C3a concentrations were similar between AD and aged controls, but threefold higher than in younger controls (p < 0.05 vs. both groups). A similar pattern was found with SC5b-9, though the increase was only twofold and statistically significant only for AD vs. younger controls. These results suggest that an increased generation of complement proteins in localized areas of the AD brain does not result in elevated concentrations of these proteins in CSF, compared with age-matched controls. Increased C3a (and, to a lesser extent, SC5b-9) in aged controls may be due to increased complement activation, increased central nervous system production, and/or blood-brain barrier leakage of these proteins.
Impairments of memory storage and retrieval produced by diazepam (2.5 mg, 5 mg, and 10 mg) in normal elderly individuals were compared to those observed in patients with primary degenerative dementia tested under nondrug conditions. The highest diazepam dose affected retrieval as well as storage processes in Buschke's "selective reminding" task, producing impairments qualitatively similar to those shown by demented patients. All diazepam doses impaired Buschke task performance in the normal elderly individuals; normal young subjects, in contrast, showed no impairment with a low (2.5 mg) diazepam dose.