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Fibril-induced neurodegenerative disorders in an Aβ-mutant Drosophila model: therapeutic targeting using ammonium molybdate.

Abstract
The ability of polyanionic molybdate to inhibit and degrade protein fibrils both in vitro (insulin protein) and in vivo (Drosophila fly model) has been demonstrated. We establish the disappearance of fibrillar structures and recovery from neurodegenerative disorders in molybdate-treated Aβ42-mutant Drosophila flies as compared to the untreated ones, corroborating the therapeutic ability of ammonium molybdate towards the treatment of Alzheimer's disease.
AuthorsSudipa Manna , Puja Karmakar , Bikash Kisan , Monalisa Mishra , Nilotpal Barooah , Achikanath C Bhasikuttan , Jyotirmayee Mohanty
JournalChemical communications (Cambridge, England) (Chem Commun (Camb)) Vol. 57 Issue 68 Pg. 8488-8491 (Sep 04 2021) ISSN: 1364-548X [Electronic] England
PMID34350921 (Publication Type: Journal Article)
Chemical References
  • Amyloid
  • Amyloid beta-Peptides
  • Drosophila Proteins
  • Peptide Fragments
  • amyloid beta-protein (1-42)
  • Molybdenum
  • ammonium molybdate
Topics
  • Amyloid (chemistry)
  • Amyloid beta-Peptides (genetics, metabolism)
  • Animals
  • Drosophila Proteins (genetics, metabolism)
  • Drosophila melanogaster
  • Drug Delivery Systems
  • Humans
  • Molybdenum (pharmacology)
  • Neurodegenerative Diseases (drug therapy, genetics, pathology)
  • Peptide Fragments (metabolism)

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