<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Llorach-Pares L</submitter><funding>Generalitat de Catalunya</funding><pagination>E386</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6213646</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(10)</volume><pubmed_abstract>Alzheimer's disease (AD) is becoming one of the most disturbing health and socioeconomic problems nowadays, as it is a neurodegenerative pathology with no treatment, which is expected to grow further due to population ageing. Actual treatments for AD produce only a modest amelioration of symptoms, although there is a constant ongoing research of new therapeutic strategies oriented to improve the amelioration of the symptoms, and even to completely cure the disease. A principal feature of AD is the presence of neurofibrillary tangles (NFT) induced by the aberrant phosphorylation of the microtubule-associated protein tau in the brains of affected individuals. Glycogen synthetase kinase-3 beta (GSK3β), casein kinase 1 delta (CK1δ), dual-specificity tyrosine phosphorylation regulated kinase 1A</pubmed_abstract><journal>Marine drugs</journal><pubmed_title>Kororamides, Convolutamines, and Indole Derivatives as Possible Tau and Dual-Specificity Kinase Inhibitors for Alzheimer's Disease: A Computational Study.</pubmed_title><pmcid>PMC6213646</pmcid><funding_grant_id>DI 2016-051</funding_grant_id><pubmed_authors>Sanchez-Martinez M</pubmed_authors><pubmed_authors>Avila C</pubmed_authors><pubmed_authors>Llorach-Pares L</pubmed_authors><pubmed_authors>Nonell-Canals A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Kororamides, Convolutamines, and Indole Derivatives as Possible Tau and Dual-Specificity Kinase Inhibitors for Alzheimer's Disease: A Computational Study.</name><description>Alzheimer's disease (AD) is becoming one of the most disturbing health and socioeconomic problems nowadays, as it is a neurodegenerative pathology with no treatment, which is expected to grow further due to population ageing. Actual treatments for AD produce only a modest amelioration of symptoms, although there is a constant ongoing research of new therapeutic strategies oriented to improve the amelioration of the symptoms, and even to completely cure the disease. A principal feature of AD is the presence of neurofibrillary tangles (NFT) induced by the aberrant phosphorylation of the microtubule-associated protein tau in the brains of affected individuals. Glycogen synthetase kinase-3 beta (GSK3β), casein kinase 1 delta (CK1δ), dual-specificity tyrosine phosphorylation regulated kinase 1A</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Oct</publication><modification>2025-04-04T09:14:30.535Z</modification><creation>2019-03-27T00:06:31Z</creation></dates><accession>S-EPMC6213646</accession><cross_references><pubmed>30332805</pubmed><doi>10.3390/md16100386</doi></cross_references></HashMap>