Literature DB >> 2148772

Small cerebral hemispheres in adults with Down's syndrome: contributions of developmental arrest and lesions of Alzheimer's disease.

S M de la Monte1, E T Hedley-Whyte.   

Abstract

Morphometric analysis was used to measure cross-sectional areas of cerebral structures in middle-aged patients with Down's syndrome (N = 5) for comparison with data obtained from individuals with senile dementia of the Alzheimer type (N = 16) and neuropathologically normal controls (N = 14). Down's syndrome was distinguished from Alzheimer's disease by the 19% lower mean brain weight which was associated with more pronounced reductions in the areas of both cortex and white matter. However, the differences were most striking in the anterior frontal and anterior temporal regions where the effects of arrested neurodevelopment are grossly evident. In addition, in Down's syndrome the amygdala was significantly smaller than in Alzheimer's disease. In both Down's syndrome and Alzheimer's disease, shrinkage of the cortical ribbon was associated with abundant neuritic plaques and neurofibrillary tangles, while white matter atrophy was associated with histopathological evidence of axonal degeneration. These findings suggest that in Down's syndrome the reduction in volume in the posterior portion of the cerebrum relative to controls is largely due to acquired lesions of Alzheimer's disease, whereas anteriorly and within certain subcortical nuclei, the effects of both Alzheimer's disease and arrested neurodevelopment are manifested. Moreover, the finding of white matter lesions in Down's syndrome corroborates the notion that white matter degeneration is a fundamental component of the Alzheimer's disease process.

Entities:  

Mesh:

Year:  1990        PMID: 2148772     DOI: 10.1097/00005072-199009000-00006

Source DB:  PubMed          Journal:  J Neuropathol Exp Neurol        ISSN: 0022-3069            Impact factor:   3.685


  6 in total

1.  Gene network disruptions and neurogenesis defects in the adult Ts1Cje mouse model of Down syndrome.

Authors:  Chelsee A Hewitt; King-Hwa Ling; Tobias D Merson; Ken M Simpson; Matthew E Ritchie; Sarah L King; Melanie A Pritchard; Gordon K Smyth; Tim Thomas; Hamish S Scott; Anne K Voss
Journal:  PLoS One       Date:  2010-07-16       Impact factor: 3.240

2.  The Down syndrome brain in the presence and absence of fibrillar β-amyloidosis.

Authors:  Tiina Annus; Liam R Wilson; Julio Acosta-Cabronero; Arturo Cardenas-Blanco; Young T Hong; Tim D Fryer; Jonathan P Coles; David K Menon; Shahid H Zaman; Anthony J Holland; Peter J Nestor
Journal:  Neurobiol Aging       Date:  2017-01-17       Impact factor: 4.673

3.  Altered expression of insulin-degrading enzyme and regulator of calcineurin in the rat intracerebral streptozotocin model and human apolipoprotein E-ε4-associated Alzheimer's disease.

Authors:  Büşra Delikkaya; Natalia Moriel; Ming Tong; Gina Gallucci; Suzanne M de la Monte
Journal:  Alzheimers Dement (Amst)       Date:  2019-05-15

4.  Cerebellar Calcium-Binding Protein and Neurotrophin Receptor Defects in Down Syndrome and Alzheimer's Disease.

Authors:  Jennifer C Miguel; Sylvia E Perez; Michael Malek-Ahmadi; Elliott J Mufson
Journal:  Front Aging Neurosci       Date:  2021-03-12       Impact factor: 5.750

5.  Developmental deficits and staging of dynamics of age associated Alzheimer's disease neurodegeneration and neuronal loss in subjects with Down syndrome.

Authors:  Jerzy Wegiel; Michael Flory; Izabela Kuchna; Krzysztof Nowicki; Jarek Wegiel; Shuang Yong Ma; Nanbert Zhong; Teresa Wierzba Bobrowicz; Mony de Leon; Florence Lai; Wayne P Silverman; Thomas Wisniewski
Journal:  Acta Neuropathol Commun       Date:  2022-01-04       Impact factor: 7.801

6.  Developmental patterns of DR6 in normal human hippocampus and in Down syndrome.

Authors:  Anand Iyer; Jackelien van Scheppingen; Jasper Anink; Ivan Milenkovic; Gabor G Kovács; Eleonora Aronica
Journal:  J Neurodev Disord       Date:  2013-04-24       Impact factor: 4.025

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.