Key result
Alzheimer disease fibroblasts show a ~3-fold elevation in bradykinin receptor density versus controls.
Why the study?
Alterations in signal transduction systems in Alzheimer's disease may have pathophysiological significance, but the phosphoinositide cascade response to bradykinin in AD fibroblasts was not well characterized.
Population
Cultured fibroblasts from Alzheimer's disease patients and age-matched controls
Comparison
Bradykinin and Prostaglandin E1 stimulation in AD vs control fibroblasts
Design
Case-control study
Authors
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Bradykinin receptor changes in AD fibroblasts are hypothesis-generating; leaves open any role in pathogenesis or therapy.
Case-Control
Absolute Event Rate: 186.8% vs 57.2%
Elevated Ins(1,4,5)P3 production in response to bradykinin in Alzheimer's disease fibroblasts correlates with an increase in bradykinin receptor numbers.
Huang et al. (1995) conducted a case-control in Alzheimer's disease. Alzheimer's disease vs. Age-matched controls was evaluated on Bradykinin receptor number (Bmax). Fibroblasts from Alzheimer's disease patients had significantly elevated bradykinin receptor numbers (186.8 vs 57.2 fmol/mg protein) and increased Ins(1,4,5)P3 production compared to controls.
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