RNA Metabolism in Human Brain During Aging and in Alzheimer’s Disease: Rna Synthesis in the Nuclei Isolated from Postmortem Brain Tissue

1992 ◽  
pp. 397-406
Author(s):  
Elizabeth M. Sajdel-Sulkowska
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Brain Tissue ◽  
Rna Synthesis ◽  
Rna Metabolism ◽  
Postmortem Brain ◽  
Postmortem Brain Tissue

P3-126: USING RNA-SEQ TO IDENTIFY RNA EDITING IN CONTROL AND ALZHEIMER'S DISEASE POSTMORTEM BRAIN TISSUE

2006 ◽  
Vol 14 (7S_Part_21) ◽  
pp. P1115-P1116
Author(s):  
Sharvari Vadeyar ◽  
Francesca North ◽  
James Turton ◽  
Tamar Guetta-Baranes ◽  
Sally Chappell ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Tissue ◽  
Rna Editing ◽  
Postmortem Brain ◽  
Rna Seq ◽  
Postmortem Brain Tissue

Amyloid binding properties of curcumin analogues in Alzheimer’s disease postmortem brain tissue

2016 ◽  
Vol 630 ◽  
pp. 183-188 ◽  
Author(s):  
Emma R. Veldman ◽  
Zhisheng Jia ◽  
Christer Halldin ◽  
Marie M. Svedberg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Tissue ◽  
Postmortem Brain ◽  
Binding Properties ◽  
Curcumin Analogues ◽  
Postmortem Brain Tissue

scholarly journals Correlation of proton transverse relaxation rates (R2) with iron concentrations in postmortem brain tissue from alzheimer's disease patients

2006 ◽  
Vol 57 (1) ◽  
pp. 172-180 ◽  
Author(s):  
Michael J. House ◽  
Timothy G. St. Pierre ◽  
Kris V. Kowdley ◽  
Thomas Montine ◽  
James Connor ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Tissue ◽  
Postmortem Brain ◽  
Relaxation Rates ◽  
Transverse Relaxation ◽  
Postmortem Brain Tissue ◽  
Iron Concentrations

Relevance of a Truncated PRESENILIN 2 Transcript to Alzheimer’s Disease and Neurodegeneration

2021 ◽  
Vol 80 (4) ◽  
pp. 1479-1489
Author(s):  
Seyyed Hani Moussavi Nik ◽  
Tenielle Porter ◽  
Morgan Newman ◽  
Benjamin Bartlett ◽  
Imran Khan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Tissue ◽  
Linear Regression Analysis ◽  
Digital Pcr ◽  
Postmortem Brain ◽  
Imaging Biomarker ◽  
Control Group ◽  
Transcript Levels ◽  
Postmortem Brain Tissue

Background: The PRESENILIN genes (PSEN1, PSEN2) encoding for their respective proteins have critical roles in many aspects of Alzheimer’s disease (AD) pathogenesis. The PS2V transcript of PSEN2 encodes a truncated protein and is upregulated in AD brains; however, its relevance to AD and disease progression remains to be determined. Objective: Assess transcript levels in postmortem AD and non-AD brain tissue and in lymphocytes collected under the Australian Imaging Biomarker and Lifestyle (AIBL) study. Methods: Full length PSEN2 and PS2V transcript levels were assessed by quantitative digital PCR in postmortem brain tissue (frontal cortex and hippocampus) from control, AD, frontotemporal dementia (FTD), and Lewy body dementia (LBD). Transcript levels were also assessed in lymphocytes obtained from the Perth subset of the AIBL study (n = 160). Linear regression analysis was used to assess correlations between transcript copy number and brain volume and neocortical amyloid load. Results: PS2V levels increased in AD postmortem brain but PS2V was also present at significant levels in FTD and LBD brains. PS2V transcript was detected in lymphocytes and PS2V/PSEN2 ratios were increased in mild cognitive impairment (p = 0.024) and AD (p = 0.019) groups compared to control group. Increased ratios were significantly correlated with hippocampal volumes only (n = 62, β= –0.269, p = 0.03). Conclusion: Taken together, these results suggest that PS2V may be a marker of overall neurodegeneration.

BACE1 mRNA Expression in Alzheimer's Disease Postmortem Brain Tissue

2011 ◽  
Vol 22 (4) ◽  
pp. 1111-1122 ◽  
Author(s):  
David T.R. Coulson ◽  
Nancy Beyer ◽  
Joe G. Quinn ◽  
Simon Brockbank ◽  
Jan Hellemans ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mrna Expression ◽  
Brain Tissue ◽  
Postmortem Brain ◽  
Postmortem Brain Tissue

scholarly journals Luminex-based quantification of Alzheimer’s disease neuropathologic change in formalin-fixed post-mortem human brain tissue

2018 ◽  
Vol 99 (7) ◽  
pp. 1056-1067
Author(s):  
C. Dirk Keene ◽  
Angela M. Wilson ◽  
Mitchell D. Kilgore ◽  
Lauren T. Bruner ◽  
Nadia O. Postupna ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Brain Tissue ◽  
Post Mortem ◽  
Human Brain Tissue ◽  
Formalin Fixed

scholarly journals The APOE ε4/ε4 Genotype Potentiates Vascular Fibrin(Ogen) Deposition in Amyloid-Laden Vessels in the Brains of Alzheimer's Disease Patients

2013 ◽  
Vol 33 (8) ◽  
pp. 1251-1258 ◽  
Author(s):  
Karin Hultman ◽  
Sidney Strickland ◽  
Erin H Norris
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Critical Role ◽  
Apoe Genotype ◽  
Postmortem Brain ◽  
Amyloid Angiopathy ◽  
Apoe Ε4 ◽  
Cerebrovascular Dysfunction ◽  
Postmortem Brain Tissue ◽  
Clotting Protein

Evidence indicates a critical role for cerebrovascular dysfunction in Alzheimer's disease (AD) pathophysiology. We have shown that fibrin(ogen), the principal blood-clotting protein, is deposited in the AD neurovasculature and interacts with beta-amyloid (Ab), resulting in increased formation of blood clots. As apolipoprotein E (ApoE), a lipid-transporting protein with three human isoforms (E2, E3, and E4), also binds to Aβ, we hypothesized that ApoE and fibrin(ogen) may have a combined effect on the vascular pathophysiology in AD. We assessed whether APOE genotype differentially influences vascular fibrin(ogen) deposition in postmortem brain tissue using immunohistochemistry. An increased deposition of fibrin(ogen) was observed in AD cases compared with non-demented controls, and there was a strong correlation between cerebral amyloid angiopathy (CAA) severity and fibrin(ogen) deposition. Moreover, brains from AD cases homozygous for APOE ε4 showed increased deposition of fibrin(ogen), specifically in CAA- and oligomeric Aβ-positive vessels compared with AD APOE ε2 and ε3 allele carriers, an effect that was not directly linked to CAA severity and cerebrovascular atherosclerosis. These data further support a role for fibrin(ogen) in AD pathophysiology and link the APOE ε4/ε4 genotype with increased thrombosis and/or impaired fibrinolysis in the human AD brain.

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