Disturbed neurotransmitter transporter expression in Alzheimer's disease brain.

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  • Additional Information
    • Source:
      Publisher: IOS Press Country of Publication: United States NLM ID: 9814863 Publication Model: Print Cited Medium: Internet ISSN: 1875-8908 (Electronic) Linking ISSN: 13872877 NLM ISO Abbreviation: J Alzheimers Dis Subsets: MEDLINE
    • Publication Information:
      Original Publication: Amsterdam ; Washington : IOS Press, c1998-
    • Subject Terms:
      Brain Chemistry*/genetics; Alzheimer Disease/*metabolism ; Neurotransmitter Transport Proteins/*biosynthesis; Aged ; Aged, 80 and over ; Aging/metabolism ; Alzheimer Disease/genetics ; Amyloid beta-Peptides/metabolism ; Blotting, Western ; Female ; Humans ; Male ; Membranes/chemistry ; Membranes/metabolism ; Middle Aged ; Neurotransmitter Transport Proteins/genetics ; Plaque, Amyloid/pathology ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/pathology ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction
    • Abstract:
      Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory loss and behavioral and psychological symptoms of dementia. An imbalance of different neurotransmitters--glutamate, acetylcholine, dopamine, and serotonin--has been proposed as the neurobiological basis of behavioral symptoms in AD. The molecular changes associated with neurotransmission imbalance in AD are not clear. We hypothesized that altered reuptake of neurotransmitters by vesicular glutamate transporters (VGLUTs), excitatory amino acid transporters (EAATs), the vesicular acetylcholine transporter (VAChT), the serotonin reuptake transporter (SERT), or the dopamine reuptake transporter (DAT) are involved in the neurotransmission imbalance in AD. We tested this hypothesis by examining protein and mRNA levels of these transporters in postmortem prefrontal cortex from 10 AD patients and 10 matched non-AD controls. Compared with controls, protein and mRNA levels of VGLUTs, EAAT1-3, VAChT, and SERT were reduced significantly in AD. Expression of DAT and catechol O-methyltransferase was unchanged. Reduced VGLUTs and EAATs may contribute to an alteration in glutamatergic recycling, and reduced SERT could exacerbate depressive symptoms in AD. The reduced VAChT expression could contribute to the recognized cholinergic deficit in AD. Altered neurotransmitter transporters could contribute to the pathophysiology of AD and are potential targets for therapy.
    • Comments:
      Retraction in: J Alzheimers Dis. 2016 Nov 1;55(1):445. doi: 10.3233/JAD-179001. (PMID: 27814301)
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    • Grant Information:
      R24 MH068855 United States MH NIMH NIH HHS; Z01 AG000148 United States ImNIH Intramural NIH HHS; R24MH068855 United States MH NIMH NIH HHS
    • Accession Number:
      0 (Amyloid beta-Peptides)
      0 (Neurotransmitter Transport Proteins)
      0 (RNA, Messenger)
    • Publication Date:
      Date Created: 20110712 Date Completed: 20120126 Latest Revision: 20241025
    • Publication Date:
      20241025
    • Accession Number:
      PMC3188700
    • Accession Number:
      10.3233/JAD-2011-110002
    • Accession Number:
      21743130