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| Home > Articles > Published articles > Monoaminergic impairment in Down syndrome with Alzheimer's disease compared to early-onset Alzheimer's disease |
(Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium) (Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium) (Fundació Catalana Síndrome de Down) (Fundació Catalana Síndrome de Down) (Institut d'Investigacions Biomèdiques August Pi i Sunyer) (Fundació Catalana Síndrome de Down) (Institut d'Investigació Biomèdica Sant Pau) (Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium) (Institut d'Investigació Biomèdica Sant Pau) (Fundació Catalana Síndrome de Down) (University Hospital Antwerp (Bèlgica))| Date: | 2017 |
| Abstract: | People with Down syndrome (DS) are at high risk for Alzheimer's disease (AD). Defects in monoamine neurotransmitter systems are implicated in DS and AD but have not been comprehensively studied in DS. Noradrenaline, adrenaline, and their metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG); dopamine and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid; and serotonin and its metabolite 5-hydroxyindoleacetic acid were quantified in 15 brain regions of DS without AD (DS, n = 4), DS with AD (DS+AD, n = 17), early-onset AD (EOAD, n = 11) patients, and healthy non-DS controls (n = 10) in the general population. Moreover, monoaminergic concentrations were determined in cerebrospinal fluid (CSF)/plasma samples of DS (n = 37/149), DS with prodromal AD (DS+pAD, n = 13/36), and DS+AD (n = 18/40). In brain, noradrenergic and serotonergic compounds were overall reduced in DS+AD versus EOAD, while the dopaminergic system showed a bidirectional change. For DS versus non-DS controls, significantly decreased MHPG levels were noted in various brain regions, though to a lesser extent than for DS+AD versus EOAD. Apart from DOPAC, CSF/plasma concentrations were not altered between groups. Monoamine neurotransmitters and metabolites were evidently impacted in DS, DS+AD, and EOAD. DS and DS+AD presented a remarkably similar monoaminergic profile, possibly related to early deposition of amyloid pathology in DS. To confirm whether monoaminergic alterations are indeed due to early amyloid β accumulation, future avenues include positron emission tomography studies of monoaminergic neurotransmission in relation to amyloid deposition, as well as relating monoaminergic concentrations to CSF/plasma levels of amyloid β and tau within individuals. |
| Grants: | Instituto de Salud Carlos III CM14-00029 Instituto de Salud Carlos III PI13-01532 Instituto de Salud Carlos III PI11-02425 Instituto de Salud Carlos III PI14-01126 |
| Note: | Altres ajuts: Fundacio Bancaria La Caixa, Marató de TV3 (20141210), Grifols Foundation, Generalitat de Catalunya 2014SGR-0235,Fundació Catalana de Sındrome de Down (FCSD), Interuniversity Poles of Attraction of the Belgian Federal Science Policy Office/IAP P7/16, Belgian Foundation for Alzheimer Research/SAO-FRA 15002. |
| Rights: | Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.  |
| Language: | Anglès |
| Document: | Article ; recerca ; Versió publicada |
| Subject: | Alzheimer's disease ; Cerebrospinal fluid ; Dementia ; Dopamine ; Down syndrome ; Monoamines ; MHPG ; Neurotransmitter ; Noradrenaline ; Plasma ; Serotonin ; Trisomy 21 |
| Published in: | Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring, Vol. 10 (november 2017) , p. 99-111, ISSN 2352-8729 |
