Differential distribution of laminins in Alzheimer disease and normal human brain tissue

2002 ◽  
Vol 69 (2) ◽  
pp. 243-256 ◽  
Author(s):  
Edouard Palu ◽  
P�ivi Liesi
2002 ◽  
Vol 176 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Fumiaki Mori ◽  
Kunikazu Tanji ◽  
Makoto Yoshimoto ◽  
Hitoshi Takahashi ◽  
Koichi Wakabayashi

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Tyler C. Hammond ◽  
Xin Xing ◽  
Peter T. Nelson ◽  
Stephanie Ham ◽  
Ai‐Ling Lin

1997 ◽  
Vol 770 (1-2) ◽  
pp. 307-309 ◽  
Author(s):  
Seiichi Haga ◽  
Masahiro Yoshimura ◽  
Yumiko Motoi ◽  
Kunimasa Arima ◽  
Takako Aizawa ◽  
...  

1994 ◽  
Vol 169 (4) ◽  
pp. 943-944 ◽  
Author(s):  
M. Luppi ◽  
P. Barozzi ◽  
A. Maiorana ◽  
R. Marasca ◽  
G. Torelli

2018 ◽  
Vol 10 (4) ◽  
Author(s):  
Michael A. Meyer

In view of recent data on the linkage of Gas7 protein to schizophrenia, and in view of its role in neurite outgrowth, histochemical localization of the Gas7 protein was studied in normal human brain tissue using an online tissue atlas. Selective localization to neurons in the cerebral cortex was found with moderate levels in the hippocampus and caudate, but fairly low levels were noted within the human cerebellum and was limited to small granule cells as well as the neuropil of the cerebellar molecular layers. Despite this low intensity histochemical localization in the cerebellum, molecular data indicate a substantially large number of RNA transcripts in the cerebellum that exceeded the cerebral cortex as determined by sequencing studies.


2018 ◽  
Vol 103 (5) ◽  
pp. 1818-1826 ◽  
Author(s):  
Elizabeth A McAninch ◽  
Kumar B Rajan ◽  
Denis A Evans ◽  
Sungro Jo ◽  
Layal Chaker ◽  
...  

Abstract Context A common single nucleotide polymorphism in DIO2, Thr92AlaD2, has been associated with a transcriptome typically found in neurodegenerative diseases in postmortem human brain tissue. Objective To determine whether Thr92AlaD2 is associated with incident Alzheimer disease (AD). Design Population-based study; human brain tissue microarray. Setting Community-based cohorts from Chicago and northeastern Illinois and religious clergymen from across the United States constituted the primary population. A representative sample of the U.S. population was used for secondary analyses. Participants 3054 African Americans (AAs) and 9304 European Americans (EAs). Main Outcome Measure Incident AD. Results In the primary population, AAs with Thr92AlaD2 had 1.3 times [95% confidence interval (CI), 1.02 to 1.68; P = 0.048] greater odds of developing AD. AAs from a second population with Thr92AlaD2 showed a trend toward increased odds of dementia (odds ratio, 1.33; 95% CI, 0.99 to 1.78; P = 0.06) and 1.35 times greater odds of developing cognitive impairment not demented (CIND; 95% CI, 1.09 to 1.67; P = 0.006). Meta-analysis showed that AAs with Thr92AlaD2 had 1.3 times increased odds of developing AD/dementia (95% CI, 1.07 to 1.58; P = 0.008). In EAs, no association was found between Thr92AlaD2 and AD, dementia, or CIND. Microarray of AA brain tissue identified transcriptional patterns linked to AD pathogenesis. Conclusions Thr92AlaD2 was associated with molecular markers known to underlie AD pathogenesis in AAs, translating to an observed phenotype of increased odds of developing AD/dementia in AAs in these populations. Thr92AlaD2 might represent one factor contributing to racial discrepancies in incident AD.


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