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Kallikrein-kinin system mediated inflammation in Alzheimer's disease in vivo.
Curr Alzheimer Res. 2011 Feb; 8(1):59-66.CA

Abstract

The Kallikrein-Kinin System (KKS) has been associated to inflammatory and immunogenic responses in the peripheral and central nervous system by the activation of two receptors, namely B1 receptor and B2 receptor. The B1 receptor is absent or under-expressed in physiological conditions, being up-regulated during tissue injury or in the presence of cytokines. The B2 receptor is constitutive and mediates most of the biological effects of kinins. Some authors suggest a link between the KKS and the neuroinflammation in Alzheimer's disease (AD). We have recently described an increase in bradykinin (BK) in the cerebrospinal fluid and in densities of B1 and B2 receptors in brain areas related to memory, after chronic infusion of amyloid-beta (Aβ) peptide in rats, which was accompanied by memory disruption and neuronal loss. Mice lacking B1 or B2 receptors presented reduced cognitive deficits related to the learning process, after acute intracerebroventricular (i.c.v). administration of Aβ. Nevertheless, our group showed an early disruption of cognitive function by i.c.v. chronic infusion of Aβ after a learned task, in the knock-out B2 mice. This suggests a neuroprotective role for B2 receptors. In knock-out B1 mice the memory disruption was absent, implying the participation of this receptor in neurodegenerative processes. The acute or chronic infusion of Aβ can lead to different responses of the brain tissue. In this way, the proper involvement of KKS on neuroinflammation in AD probably depends on the amount of Aβ injected. Though, BK applied to neurons can exert inflammatory effects, whereas in glial cells, BK can have a potential protective role for neurons, by inhibiting proinflammatory cytokines. This review discusses this duality concerning the KKS and neuroinflammation in AD in vivo.

Authors+Show Affiliations

School of Arts, Sciences and Humanities, Universidade de Sao Paulo, SP, Brazil.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

21143155

Citation

Viel, T A., and H S. Buck. "Kallikrein-kinin System Mediated Inflammation in Alzheimer's Disease in Vivo." Current Alzheimer Research, vol. 8, no. 1, 2011, pp. 59-66.
Viel TA, Buck HS. Kallikrein-kinin system mediated inflammation in Alzheimer's disease in vivo. Curr Alzheimer Res. 2011;8(1):59-66.
Viel, T. A., & Buck, H. S. (2011). Kallikrein-kinin system mediated inflammation in Alzheimer's disease in vivo. Current Alzheimer Research, 8(1), 59-66.
Viel TA, Buck HS. Kallikrein-kinin System Mediated Inflammation in Alzheimer's Disease in Vivo. Curr Alzheimer Res. 2011;8(1):59-66. PubMed PMID: 21143155.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Kallikrein-kinin system mediated inflammation in Alzheimer's disease in vivo. AU - Viel,T A, AU - Buck,H S, PY - 2010/09/10/received PY - 2010/10/05/accepted PY - 2010/12/15/entrez PY - 2010/12/15/pubmed PY - 2011/7/2/medline SP - 59 EP - 66 JF - Current Alzheimer research JO - Curr Alzheimer Res VL - 8 IS - 1 N2 - The Kallikrein-Kinin System (KKS) has been associated to inflammatory and immunogenic responses in the peripheral and central nervous system by the activation of two receptors, namely B1 receptor and B2 receptor. The B1 receptor is absent or under-expressed in physiological conditions, being up-regulated during tissue injury or in the presence of cytokines. The B2 receptor is constitutive and mediates most of the biological effects of kinins. Some authors suggest a link between the KKS and the neuroinflammation in Alzheimer's disease (AD). We have recently described an increase in bradykinin (BK) in the cerebrospinal fluid and in densities of B1 and B2 receptors in brain areas related to memory, after chronic infusion of amyloid-beta (Aβ) peptide in rats, which was accompanied by memory disruption and neuronal loss. Mice lacking B1 or B2 receptors presented reduced cognitive deficits related to the learning process, after acute intracerebroventricular (i.c.v). administration of Aβ. Nevertheless, our group showed an early disruption of cognitive function by i.c.v. chronic infusion of Aβ after a learned task, in the knock-out B2 mice. This suggests a neuroprotective role for B2 receptors. In knock-out B1 mice the memory disruption was absent, implying the participation of this receptor in neurodegenerative processes. The acute or chronic infusion of Aβ can lead to different responses of the brain tissue. In this way, the proper involvement of KKS on neuroinflammation in AD probably depends on the amount of Aβ injected. Though, BK applied to neurons can exert inflammatory effects, whereas in glial cells, BK can have a potential protective role for neurons, by inhibiting proinflammatory cytokines. This review discusses this duality concerning the KKS and neuroinflammation in AD in vivo. SN - 1875-5828 UR - https://www.unboundmedicine.com/medline/citation/21143155/Kallikrein_kinin_system_mediated_inflammation_in_Alzheimer's_disease_in_vivo_ L2 - http://www.eurekaselect.com/87518/article DB - PRIME DP - Unbound Medicine ER -