ArticleAlzheimer's & dementia (Amsterdam, Netherlands)2018
Monoaminergic impairment in Down syndrome with Alzheimer's disease compared to early-onset Alzheimer's disease.
Article in Alzheimer's & dementia (Amsterdam, Netherlands), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.
- Catecholamines in Alzheimer's Disease: A Systematic Review and Meta-Analysis.Frontiers in aging neuroscience · 2020Pooled it
- Dopamine and Dopamine Receptors in Alzheimer's Disease: A Systematic Review and Network Meta-Analysis.Frontiers in aging neuroscience · 2019Pooled it
- The association between APOE 𝜀4 carrierships and the detection of amyloid positivity using an Alzheimer's disease proteomic blood test in asymptomatic Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Charting the future: current and future directions in translational research for individuals with Down syndrome.Journal of neurodevelopmental disorders · 2025Review
- Disease-specific neuropathological alterations of the locus coeruleus in Alzheimer's disease, Down syndrome, and Parkinson's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Monoamine alterations in Alzheimer's disease and their implications in comorbid neuropsychiatric symptoms.GeroScience · 2025Review
- Deciphering the Functions of Raphe-Hippocampal Serotonergic and Glutamatergic Circuits and Their Deficits in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Exploring peripheral fluid biomarkers for early detection of Alzheimer's disease in Down syndrome: A literature review.Heliyon · 2025Review
- Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine β-synthase, HGeroScience · 2024Article
- Dopamine-related oxidative stress and mitochondrial dysfunction in dopaminergic neurons differentiated from deciduous teeth-derived stem cells of children with Down syndrome.FASEB bioAdvances · 2022Article
- Frontal cortex and striatal cellular and molecular pathobiology in individuals with Down syndrome with and without dementia.Acta neuropathologica · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPeople 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.
methodsNoradrenaline, 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).
resultsIn 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. DISCUSSION: 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.