Literature DB >> 25125458

Global N-acetylaspartate in normal subjects, mild cognitive impairment and Alzheimer's disease patients.

Lidia Glodzik1, Marc Sollberger2, Achim Gass3, Amit Gokhale4, Henry Rusinek4, James S Babb4, Jochen G Hirsch3, Michael Amann3, Andreas U Monsch5, Oded Gonen4.   

Abstract

BACKGROUND: Mild cognitive impairment (MCI) is an intermediary state on the way to Alzheimer's disease (AD). Little is known about whole brain concentration of the neuronal marker, N-acetylaspartate (NAA) in MCI patients.
OBJECTIVE: To test the hypothesis that since MCI and AD are both neurodegenerative, quantification of the NAA in their whole brain (WBNAA) could differentiate them from cognitively-intact matched controls.
METHODS: Proton MR spectroscopy to quantify the WBNAA was applied to 197 subjects (86 females) 72.6 ± 8.4 years old (mean ± standard deviation). Of these, 102 were cognitively intact, 42 diagnosed as MCI, and 53 as probable AD. Their WBNAA amounts were converted into absolute concentration by dividing with the brain volume segmented from the MRI that also yielded the fractional brain volume (fBPV), an atrophy metric.
RESULTS: WBNAA concentration of MCI and AD patients (10.5 ± 3.0 and 10.1 ± 2.9 mM) were not significantly different (p = 0.85). They were, however, highly significantly 25-29% lower than the 14.1 ± 2.4 mM of normal matched controls (p < 10-4). The fBPV of MCI and AD patients (72.9 ± 4.9 and 69.9 ± 4.7%) differed significantly from each other (4%, p = 0.02) and both were significantly lower than the 74.6 ± 4.4% of normal elderly (2%, p = 0.003 for MCI; 6%, p < 10-4 for AD). ROC curve analysis has shown WBNAA to have 70.5% sensitivity and 84.3% specificity to differentiate MCI or AD patients from normal elderly versus just 68.4 and 65.7% for fBPV.
CONCLUSION: Low WBNAA in MCI patients compared with cognitively normal contemporaries may indicate early neuronal damage accumulation and supports the notion of MCI as an early stage of AD. It also suggests WBNAA as a potential marker of early AD pathology.

Entities:  

Keywords:  Alzheimer's disease; N-acetylaspartate; magnetic resonance spectroscopy; mild cognitive impairment; normal aging

Mesh:

Substances:

Year:  2015        PMID: 25125458      PMCID: PMC4445651          DOI: 10.3233/JAD-140609

Source DB:  PubMed          Journal:  J Alzheimers Dis        ISSN: 1387-2877            Impact factor:   4.472


  45 in total

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Journal:  Proc Natl Acad Sci U S A       Date:  2001-08-28       Impact factor: 11.205

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3.  Conversion from subtypes of mild cognitive impairment to Alzheimer dementia.

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4.  Reduced medial temporal lobe N-acetylaspartate in cognitively impaired but nondemented patients.

Authors:  L L Chao; N Schuff; J H Kramer; A T Du; A A Capizzano; J O'Neill; O M Wolkowitz; W J Jagust; H C Chui; B L Miller; K Yaffe; M W Weiner
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5.  (1)H-MR spectroscopy differentiates mild cognitive impairment from normal brain aging.

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Authors:  A Falini; M Bozzali; G Magnani; G Pero; A Gambini; B Benedetti; R Mossini; M Franceschi; G Comi; G Scotti; M Filippi
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8.  Prevalence of cognitive impairment: data from the Indianapolis Study of Health and Aging.

Authors:  F W Unverzagt; S Gao; O Baiyewu; A O Ogunniyi; O Gureje; A Perkins; C L Emsley; J Dickens; R Evans; B Musick; K S Hall; S L Hui; H C Hendrie
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9.  Difference of the hippocampal and white matter microalterations in MCI patients according to the severity of subcortical vascular changes: neuropsychological correlates of diffusion tensor imaging.

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5.  Unbiased Metabolomic Investigation of Alzheimer's Disease Brain Points to Dysregulation of Mitochondrial Aspartate Metabolism.

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8.  Effects of Alterations of Post-Mortem Delay and Other Tissue-Collection Variables on Metabolite Levels in Human and Rat Brain.

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