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      1H-MRS metabolites in adults with Down syndrome: Effects of dementia

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          Abstract

          To determine if proton magnetic resonance spectroscopy ( 1H-MRS) detect differences in dementia status in adults with Down syndrome (DS), we used 1H-MRS to measure neuronal and glial metabolites in the posterior cingulate cortex in 22 adults with DS and in 15 age- and gender-matched healthy controls. We evaluated associations between 1H-MRS results and cognition among DS participants. Neuronal biomarkers, including N-acetylaspartate (NAA) and glutamate-glutamine complex (Glx), were significantly lower in DS patients with Alzheimer's should probably be changed to Alzheimer (without ' or s) through ms as per the new naming standard disease (DSAD) when compared to non-demented DS (DS) and healthy controls (CTL). Neuronal biomarkers therefore appear to reflect dementia status in DS. In contrast, all DS participants had significantly higher myo-inositol (MI), a putative glial biomarker, compared to CTL. Our data indicate that there may be an overall higher glial inflammatory component in DS compared to CTL prior to and possibly independent of developing dementia. When computing the NAA to MI ratio, we found that presence or absence of dementia could be distinguished in DS. NAA, Glx, and NAA/MI in all DS participants were correlated with scores from the Brief Praxis Test and the Severe Impairment Battery. 1H-MRS may be a useful diagnostic tool in future longitudinal studies to measure AD progression in persons with DS. In particular, NAA and the NAA/MI ratio is sensitive to the functional status of adults with DS, including prior to dementia.

          Highlights

          • •

            1H-MRS was used to compare demented and nondemented adults with Down syndrome.

          • •

            Neuronal biomarkers were lowest in demented adults with Down syndrome.

          • •

            Glial biomarkers including myoinositol were higher in demented adults with DS.

          • •

            Neuronal and glial biomarkers were correlated with cognition in Down syndrome.

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          The cholinergic system in aging and neuronal degeneration.

          Reinhard Schliebs, Thomas Arendt (2011)
          The basal forebrain cholinergic complex comprising medial septum, horizontal and vertical diagonal band of Broca, and nucleus basalis of Meynert provides the mayor cholinergic projections to the cerebral cortex and hippocampus. The cholinergic neurons of this complex have been assumed to undergo moderate degenerative changes during aging, resulting in cholinergic hypofunction that has been related to the progressing memory deficits with aging. However, the previous view of significant cholinergic cell loss during aging has been challenged. Neuronal cell loss was found predominantly in pathological aging, such as Alzheimer's disease, while normal aging is accompanied by a gradual loss of cholinergic function caused by dendritic, synaptic, and axonal degeneration as well as a decrease in trophic support. As a consequence, decrements in gene expression, impairments in intracellular signaling, and cytoskeletal transport may mediate cholinergic cell atrophy finally leading to the known age-related functional decline in the brain including aging-associated cognitive impairments. However, in pathological situations associated with cognitive deficits, such as Parkinsons's disease, Down-syndrome, progressive supranuclear palsy, Jakob-Creutzfeld disease, Korsakoff's syndrome, traumatic brain injury, significant degenerations of basal forebrain cholinergic cells have been observed. In presenile (early onset), and in the advanced stages of late-onset Alzheimer's disease (AD), a severe loss of cortical cholinergic innervation has extensively been documented. In contrast, in patients with mild cognitive impairment (MCI, a prodromal stage of AD), and early forms of AD, apparently no cholinergic neurodegeneration but a loss of cholinergic function occurs. In particular imbalances in the expression of NGF, its precursor proNGF, the high and low NGF receptors, trkA and p75NTR, respectively, changes in acetylcholine release, high-affinity choline uptake, as well as alterations in muscarinic and nicotinic acetylcholine receptor expression may contribute to the cholinergic dysfunction. These observations support the suggestion of a key role of the cholinergic system in the functional processes that lead to AD. Malfunction of the cholinergic system may be tackled pharmacologically by intervening in cholinergic as well as neurotrophic signaling cascades that have been shown to ameliorate the cholinergic deficit at early stages of the disease, and slow-down the progression. However, in contrast to many other, dementing disorders, in AD the cholinergic dysfunctions are accompanied by the occurrence of two major histopathological hallmarks such as β-amyloid plaques and neurofibrillary tangles, provoking the question whether they play a particular role in inducing or mediating cholinergic dysfunction in AD. Indeed, there is abundant evidence that β-amyloid may trigger cholinergic dysfunction through action on α7 nicotinic acetylcholine receptors, affecting NGF signaling, mediating tau phosphorylation, interacting with acetylcholinesterase, and specifically affecting the proteome in cholinergic neurons. Therefore, an early onset of an anti β-amyloid strategy may additionally be potential in preventing aging-associated cholinergic deficits and cognitive impairments. Copyright © 2010 Elsevier B.V. All rights reserved.
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            Fractionating the default mode network: distinct contributions of the ventral and dorsal posterior cingulate cortex to cognitive control.

            Robert Leech, Salwa Kamourieh, Christian F. Beckmann … (2011)
            The posterior cingulate cortex (PCC) is a central part of the default mode network (DMN) and part of the structural core of the brain. Although the PCC often shows consistent deactivation when attention is focused on external events, anatomical studies show that the region is not homogeneous, and electrophysiological recordings in nonhuman primates suggest that it is directly involved in some forms of attention. We report a functional magnetic resonance imaging study of an attentionally demanding task (either a zero- or two-back working memory task). Standard subtraction analysis within the PCC shows a relative deactivation as task difficulty increases. In contrast, a dual-regression functional connectivity analysis reveals a clear dissociation between ventral and dorsal parts of the PCC. As task difficulty increases, the ventral PCC shows reduced integration within the DMN and less anticorrelation with the cognitive control network (CCN) activated by the task. The dorsal PCC shows an opposite pattern, with increased DMN integration and more anticorrelation. At rest, the dorsal PCC also shows functional connectivity with both the DMN and attentional networks. As expected, these results provide evidence that the PCC is involved in supporting internally directed thought, as the region is more highly integrated with the DMN at low task demands. In contrast, the task-dependent increases in connectivity between the dorsal PCC and the CCN are consistent with a role for this region in modulating the dynamic interaction between these two networks controlling the efficient allocation of attention.
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              Occurrence of neuropathological changes and dementia of Alzheimer's disease in Down's syndrome.

              H M Wisniewski, K Wisniewski, Ben Wen (1985)
              One hundred brains of patients with Down's syndrome (DS) who died in institutions for chronic care were examined for clinicopathological correlation of Alzheimer's disease. Fifty-one were below and 49 were above age 30 years at death. Tissues from the right, prefrontal, and hippocampal cortices were processed for microscopy using H&E and Bodian-periodic acid-Schiff impregnation. Morphometric evaluations of plaques and tangles were carried out. Plaques or plaques and tangles were found in the brains of 56 patients with DS, 7 below age 30 and 49 above that age. A history of dementia was evident in the medical records of 15 of these patients; of these only 2 were below the age of 30. The brains of the patients with DS who also had clinical dementia had more than twenty plaques or plaques and tangles per 1.5 X 10(6) micron 2 of cortex. The numbers of plaques and tangles found in the brains of the patients with DS above the age of 30 greatly increased with age but varied from brain to brain. These observations suggest a correlation among dementia, the density of plaques and tangles, and age. All 100 brains studied showed early arrest of brain growth and brain atrophy, a condition that may have been due to prenatal arrest of neurogenesis mainly in the granular cell layers, prenatal and postnatal arrest of synaptogenesis, and early aging. Plaques and tangles developed twenty to thirty years earlier and dementia was clinically detected at least three times more frequently (20 to 30%) in DS than it is known to occur in the non-DS population.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neuroimage Clin
                Journal ID (iso-abbrev): Neuroimage Clin
                Title: NeuroImage : Clinical
                Publisher: Elsevier
                ISSN (Electronic): 2213-1582
                Publication date PMC-release: 02 June 2016
                Publication date Collection: 2016
                Publication date (Electronic): 02 June 2016
                Volume: 11
                Pages: 728-735
                Affiliations
                [a ]Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA
                [b ]Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA
                [c ]Magnetic Resonance Imaging and Spectroscopy Center, University of Kentucky, Lexington, KY, USA
                [d ]Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY, USA
                [e ]Department of Neurology, University of Kentucky, Lexington, KY, USA
                [f ]Department of Physiology, University of Kentucky, Lexington, KY, USA
                Author notes
                [* ]Corresponding author at: Sanders Brown Center on Aging, Pharmacology & Nutritional Sciences, University of Kentucky, 203 Sanders-Brown Building, 800 South Limestone Street, Lexington, KY 40536-0230, USA.Sanders Brown Center on AgingPharmacology & Nutritional SciencesUniversity of Kentucky203 Sanders-Brown Building800 South Limestone StreetLexingtonKY40536-0230USA
                [1]

                Co-senior authors.

                Article
                Publisher ID: S2213-1582(16)30099-7
                DOI: 10.1016/j.nicl.2016.06.001
                PMC ID: 4908308
                PubMed ID: 27330972
                SO-VID: 573fcd90-ee90-4c8c-a3af-efaded52383e
                Copyright © © 2016 Published by Elsevier Inc.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 2 September 2015
                Date revision received : 11 April 2016
                Date accepted : 1 June 2016
                Categories
                Subject: Regular Article

                Keywords: brief praxis test,inflammation,myoinositol,severe impairment battery,trisomy 21
                Data availability:
                Keywords: brief praxis test, inflammation, myoinositol, severe impairment battery, trisomy 21

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