Increased metabolic activity in nucleus basalis of Meynert neurons in elderly individuals with mild cognitive impairment as indicated by the size of the Golgi apparatus

被引:27
作者
Dubelaar, Elisabeth J. G.
Mufson, Elliott J.
ter Meulen, Wendela G.
Van Heerikhuize, Joop J.
Verwer, Ronald W. H.
Swaab, Dick F.
机构
[1] Netherlands Inst Brain Res, NL-1105 AZ Amsterdam, Netherlands
[2] Rush Univ, Med Ctr, Chicago, IL 60612 USA
关键词
Alzheimer disease; Braak stage; cholinergic; Golgi apparatus; metabolism; mild cognitive impairment; nucleus basalis of Meynert;
D O I
10.1097/01.jnen.0000205143.16339.cd
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
In this study, we examined the metabolic activity of nucleus basalis of Meynert (NBM) neurons in individuals clinically diagnosed with no cognitive impairment (NCI, n = 8), mild cognitive impairment (MCI, n = 9), and subjects with moderate Alzheimer disease (AD, n = 7). We used Golgi apparatus (GA) size as a measure of neuronal metabolic activity. Subjects with MCI showed increased NBM metabolic activity; they had significantly more neurons with larger GA size as compared with NCI and AD subjects. In contrast, more NBM neurons with extremely small GA sizes, indicating reduced metabolic activity, were seen in AD. When these cases were classified according to their AD pathology (Braak I-II, III-IV, or V-VI), Braak III-IV subjects showed significantly increased GA sizes, comparable with the increase in clinically diagnosed MCI, whereas in Braak V-VI, GA sizes were dramatically reduced. Of all MCI and NCI subjects with similar Braak III-IV pathology, the MCI subjects again had significantly larger GA sizes. The larger NBM neuronal GA size seen in MCI suggests increased metabolic activity, associated with both the clinical progression from NCI to MCI, and with the early stages of AD pathology.
引用
收藏
页码:257 / 266
页数:10
相关论文
共 74 条
[1]  
[Anonymous], 1997, Neurobiol Aging, V18, pS1
[2]   DISTRIBUTION OF ALZHEIMER-TYPE PATHOLOGICAL-CHANGES IN NONDEMENTED ELDERLY INDIVIDUALS MATCHES THE PATTERN IN ALZHEIMERS-DISEASE [J].
ARRIAGADA, PV ;
MARZLOFF, K ;
HYMAN, BT .
NEUROLOGY, 1992, 42 (09) :1681-1688
[3]  
Baloyannis Stavros J, 2004, Am J Alzheimers Dis Other Demen, V19, P89, DOI 10.1177/153331750401900205
[4]   Correlations between mental state and quantitative neuropathology in the Vienna longitudinal study on dementia [J].
Bancher, C ;
Jellinger, K ;
Lassmann, H ;
Fischer, P ;
Leblhuber, F .
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE, 1996, 246 (03) :137-146
[5]   Natural history of mild cognitive impairment in older persons [J].
Bennett, DA ;
Wilson, RS ;
Schneider, JA ;
Evans, DA ;
Beckett, LA ;
Aggarwal, NT ;
Barnes, LL ;
Fox, JH ;
Bach, J .
NEUROLOGY, 2002, 59 (02) :198-205
[6]   Progression to dementia in patients with isolated memory loss [J].
Bowen, J ;
Teri, L ;
Kukull, W ;
McCormick, W ;
McCurry, SM ;
Larson, EB .
LANCET, 1997, 349 (9054) :763-765
[7]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[8]   Down-regulation of trkA mRNA within nucleus basalis neurons in individuals with mild cognitive impairment and Alzheimer's disease [J].
Chu, YP ;
Cochran, EJ ;
Bennett, DA ;
Mufson, EJ ;
Kordower, JH .
JOURNAL OF COMPARATIVE NEUROLOGY, 2001, 437 (03) :296-307
[9]  
COCHRAN EJ, 1994, ACTA NEUROPATHOL, V88, P479
[10]   Reduction of cortical TrkA but not p75NTR protein in early-stage Alzheimer's disease [J].
Counts, SE ;
Nadeem, M ;
Wuu, J ;
Ginsberg, SD ;
Saragovi, HU ;
Mufson, EJ .
ANNALS OF NEUROLOGY, 2004, 56 (04) :520-531