Caetano, A. L.
Dong-Creste, K. E.
Amaral, F. A.
Monteiro-Silva, K. C.
Pesquero, J. B.
Araujo, M. S.
Montor, W. R.
Vie, T. A.
Buck, H. S.
Total Authors: 9
 Santa Casa de Sao Paulo Sch Med Sci, Dept Physiol Sci, BR-01221020 Sao Paulo, SP - Brazil
 Univ Fed Sao Paulo, Dept Biophys, BR-04021001 Sao Paulo, SP - Brazil
 Univ Fed Sao Paulo, Dept Biochem, BR-04021001 Sao Paulo, SP - Brazil
 Univ Sao Paulo, Sch Arts Sci & Humanities, BR-03828080 Sao Paulo, SP - Brazil
 Univ Sao Paulo, Inst Biomed Sci, Grad Course Pharmacol, BR-03828080 Sao Paulo, SP - Brazil
Total Affiliations: 5
Web of Science Citations:
Alzheimer's disease (AD) is characterized by cognitive decline, presence of amyloid-beta peptide (A beta) aggregates and neurofibrillary tangles. Kinins act through 91 and B2 G-protein coupled receptors (B1R and B2R). Chronic infusion of A beta peptide leads to memory impairment and increases in densities of both kinin receptors in memory processing areas. Similar memory impairment was observed in C57BL/6 mice (WTA beta) but occurred earlier in mice lacking B2R (KOB2A beta) and was absent in mice lacking B1R (KOB1A beta). Thus, the aim of this study was to evaluate the participation of B1R and B2R in A beta peptide induced cognitive deficits through the evaluation of densities of kinin receptors, synapses, cell bodies and number of A beta deposits in brain of WTA beta, KOB1A beta and KOB2A beta mice. An increase in B2R density was observed in both WTA beta and KOB1A beta in memory processing related areas. KOB1A beta showed a decrease in neuronal density and an increase in synaptic density and, in addition, an increase in A beta deposits in KOB2A beta was observed. In conclusion, memory preservation in KOB1A beta, could be due to the increase in densities of B2R, suggesting a neuroprotective role for B2R, reinforced by the increased number of A beta plaques in KOB2A beta. Our data point to B2R as a potential therapeutic target in AD. (C) 2015 Elsevier Ltd. All rights reserved. (AU)