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In-vivo histamine H3 receptor antagonism activates cellular signaling suggestive of symptomatic and disease modifying efficacy in Alzheimer's disease.
Bitner, R Scott; Markosyan, Stella; Nikkel, Arthur L; Brioni, Jorge D.
Afiliación
  • Bitner RS; Neuroscience Research, Global Pharmaceutical Research and Development, Abbott Laboratories, 100 Abbott Park Road, Abbott Park, IL 60064, USA. robert.s.bitner@abbott.com
Neuropharmacology ; 60(2-3): 460-6, 2011.
Article en En | MEDLINE | ID: mdl-21044639
Histamine H(3) receptor antagonists enhance cognition in preclinical models and have been proposed as novel therapeutics for cognitive disorders, in particular Alzheimer's disease (AD). Increased neurotransmitter (e.g. acetylcholine and histamine) release associated with this pharmacology may lead to activation of postsynaptic signaling pathways relevant to cognition and neuroprotection, such as increased phosphorylation of CREB, a transcription factor germane to cognitive function, and the inhibitory residue (Ser-9) of GSK3ß, a primary tau kinase associated with AD pathology. In the present studies, acute administration of the H(3)-antagonist ABT-239 (0.01-1.0mg/kg i.p.) increased cortical CREB and S(9)-GSK3ß phosphorylation in CD1 mice. Donepezil, while increasing CREB phosphorylation, did not increase pS(9)-GSK3ß expression in contrast to ABT-239. Continuous (2-wk) s.c. infusion of ABT-239 (0.7 mg/kg/day) normalized reduced cortical CREB and hippocampal S(9)-GSK3ß phosphorylation observed in Tg2576 (APP) AD-transgenic mice. In addition, ABT-239 infusion reversed tau hyperphosphorylation in the spinal cord and hippocampus of TAPP (tau × APP) AD-transgenic mice. Interestingly, ABT-239 produced signaling changes (pS(9)-GSK3ß) in α7 nicotinic acetylcholine receptor (nAChR) knockout mice. In contrast to wild type, these mice do not exhibit α7 nAChR agonist induced phosphorylation, thus suggesting that H(3)-antagonist-mediated signaling is not dependent on ACh-stimulated α7 nAChR activation. In summary, results of these studies suggest that ABT-239 leads to biochemical signaling that promotes cognitive performance as well as attenuation of tau hyperphosphorylation, raising the intriguing possibility that H(3) antagonists have potential for both symptomatic and disease modifying benefit in the treatment of AD.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pirrolidinas / Benzofuranos / Transducción de Señal / Membrana Celular / Receptores Histamínicos H3 / Antagonistas de los Receptores Histamínicos H3 / Enfermedad de Alzheimer Tipo de estudio: Diagnostic_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Neuropharmacology Año: 2011 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pirrolidinas / Benzofuranos / Transducción de Señal / Membrana Celular / Receptores Histamínicos H3 / Antagonistas de los Receptores Histamínicos H3 / Enfermedad de Alzheimer Tipo de estudio: Diagnostic_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Neuropharmacology Año: 2011 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido