Articles producció científica> Bioquímica i Biotecnologia

Current Research Therapeutic Strategies for Alzheimer's Disease Treatment

  • Dades identificatives

    Identificador: imarina:5129943
    Autors:
    Folch, JaumePetrov, DmitryEttcheto, MirenAbad, SoniaSanchez-Lopez, ElenaLuisa Garcia, MOlloquequi, JordiBeas-Zarate, CarlosAuladell, CarmeCamins, Antoni
    Resum:
    Alzheimer's disease (AD) currently presents one of the biggest healthcare issues in the developed countries. There is no effective treatment capable of slowing down disease progression. In recent years the main focus of research on novel pharmacotherapies was based on the amyloidogenic hypothesis of AD, which posits that the beta amyloid (A¿) peptide is chiefly responsible for cognitive impairment and neuronal death. The goal of such treatments is (a) to reduce A¿ production through the inhibition of ¿ and ¿ secretase enzymes and (b) to promote dissolution of existing cerebral A¿ plaques. However, this approach has proven to be only modestly effective. Recent studies suggest an alternative strategy centred on the inhibition of the downstream A¿ signalling, particularly at the synapse. A¿ oligomers may cause aberrant N-methyl-D-aspartate receptor (NMDAR) activation postsynaptically by forming complexes with the cell-surface prion protein (PrPC). PrPC is enriched at the neuronal postsynaptic density, where it interacts with Fyn tyrosine kinase. Fyn activation occurs when A¿ is bound to PrPC-Fyn complex. Fyn causes tyrosine phosphorylation of the NR2B subunit of metabotropic glutamate receptor 5 (mGluR5). Fyn kinase blockers masitinib and saracatinib have proven to be efficacious in treating AD symptoms in experimental mouse models of the disease.
  • Altres:

    Autor segons l'article: Folch, Jaume; Petrov, Dmitry; Ettcheto, Miren; Abad, Sonia; Sanchez-Lopez, Elena; Luisa Garcia, M; Olloquequi, Jordi; Beas-Zarate, Carlos; Auladell, Carme; Camins, Antoni
    Departament: Bioquímica i Biotecnologia
    Autor/s de la URV: Folch Lopez, Jaume
    Paraules clau: Thiazoles Synapses Serotonin 6 receptor Selective monoamine-oxidase Saracatinib Receptors, serotonin Receptors, n-methyl-d-aspartate Receptor, metabotropic glutamate 5 Quinazolines Pyridines Prpc proteins Proto-oncogene proteins c-fyn Protein kinase inhibitors Piperidines Neurons Mild cognitive impairment Mice Masitinib Intranasal insulin Humans Grm5 protein, human Gamma-secretase Fyn protein, human Double-blind Disease models, animal Central-nervous-system Brain Benzodioxoles Benzamides Avagacestat bms-708163 Animals Amyloid-beta Amyloid beta-peptides Amyloid beta protein Alzheimer disease Aggregation inhibitor therapy A-beta-oligomers
    Resum: Alzheimer's disease (AD) currently presents one of the biggest healthcare issues in the developed countries. There is no effective treatment capable of slowing down disease progression. In recent years the main focus of research on novel pharmacotherapies was based on the amyloidogenic hypothesis of AD, which posits that the beta amyloid (A¿) peptide is chiefly responsible for cognitive impairment and neuronal death. The goal of such treatments is (a) to reduce A¿ production through the inhibition of ¿ and ¿ secretase enzymes and (b) to promote dissolution of existing cerebral A¿ plaques. However, this approach has proven to be only modestly effective. Recent studies suggest an alternative strategy centred on the inhibition of the downstream A¿ signalling, particularly at the synapse. A¿ oligomers may cause aberrant N-methyl-D-aspartate receptor (NMDAR) activation postsynaptically by forming complexes with the cell-surface prion protein (PrPC). PrPC is enriched at the neuronal postsynaptic density, where it interacts with Fyn tyrosine kinase. Fyn activation occurs when A¿ is bound to PrPC-Fyn complex. Fyn causes tyrosine phosphorylation of the NR2B subunit of metabotropic glutamate receptor 5 (mGluR5). Fyn kinase blockers masitinib and saracatinib have proven to be efficacious in treating AD symptoms in experimental mouse models of the disease.
    Àrees temàtiques: Transplantation Saúde coletiva Psicología Neurosciences Neurology (clinical) Neurology Medicina veterinaria Medicina ii Medicina i Interdisciplinar Filosofía Farmacia Engenharias iv Educação física Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Ciência da computação
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 07928483
    Adreça de correu electrònic de l'autor: jaume.folch@urv.cat
    Identificador de l'autor: 0000-0002-5051-8858
    Data d'alta del registre: 2024-10-19
    Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
    Enllaç font original: https://www.hindawi.com/journals/np/2016/8501693/
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referència a l'article segons font original: Neural Plasticity. 2016 (8501693): 8501693-
    Referència de l'ítem segons les normes APA: Folch, Jaume; Petrov, Dmitry; Ettcheto, Miren; Abad, Sonia; Sanchez-Lopez, Elena; Luisa Garcia, M; Olloquequi, Jordi; Beas-Zarate, Carlos; Auladell, C (2016). Current Research Therapeutic Strategies for Alzheimer's Disease Treatment. Neural Plasticity, 2016(8501693), 8501693-. DOI: 10.1155/2016/8501693
    DOI de l'article: 10.1155/2016/8501693
    Entitat: Universitat Rovira i Virgili
    Any de publicació de la revista: 2016
    Tipus de publicació: Journal Publications
  • Paraules clau:

    Neurology,Neurology (Clinical),Neurosciences,Transplantation
    Thiazoles
    Synapses
    Serotonin 6 receptor
    Selective monoamine-oxidase
    Saracatinib
    Receptors, serotonin
    Receptors, n-methyl-d-aspartate
    Receptor, metabotropic glutamate 5
    Quinazolines
    Pyridines
    Prpc proteins
    Proto-oncogene proteins c-fyn
    Protein kinase inhibitors
    Piperidines
    Neurons
    Mild cognitive impairment
    Mice
    Masitinib
    Intranasal insulin
    Humans
    Grm5 protein, human
    Gamma-secretase
    Fyn protein, human
    Double-blind
    Disease models, animal
    Central-nervous-system
    Brain
    Benzodioxoles
    Benzamides
    Avagacestat bms-708163
    Animals
    Amyloid-beta
    Amyloid beta-peptides
    Amyloid beta protein
    Alzheimer disease
    Aggregation inhibitor therapy
    A-beta-oligomers
    Transplantation
    Saúde coletiva
    Psicología
    Neurosciences
    Neurology (clinical)
    Neurology
    Medicina veterinaria
    Medicina ii
    Medicina i
    Interdisciplinar
    Filosofía
    Farmacia
    Engenharias iv
    Educação física
    Ciências biológicas iii
    Ciências biológicas ii
    Ciências biológicas i
    Ciência da computação
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