Loss of stimulatory effect of guanosine triphosphate on [35S]GTPγS binding correlates with Alzheimer's disease neurofibrillary pathology in entorhinal cortex and CA1 hippocampal subfield

2001 ◽  
Vol 67 (3) ◽  
pp. 388-398 ◽  
Author(s):  
A. García-Jiménez ◽  
R.F. Cowburn ◽  
T.G. Ohm ◽  
H. Lasn ◽  
B. Winblad ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Neurofibrillary Pathology ◽  
Guanosine Triphosphate ◽  
Gtpγs Binding

P1-178: Early astrocytic atrophy in the Entorhinal cortex of a triple transgenic animal model of Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. S225-S225
Author(s):  
Chia-Yu Yeh ◽  
Markel Olabarria ◽  
Harun N. Noristani ◽  
Alexei Verkhratsky ◽  
Jose J. Rodriguez
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Entorhinal Cortex ◽  
Transgenic Animal ◽  
Transgenic Animal Model ◽  
Model Of Alzheimer’S Disease

Association of the CX3CR1-V249I Variant with Neurofibrillary Pathology Progression in Late-Onset Alzheimer’s Disease

2017 ◽  
Vol 55 (3) ◽  
pp. 2340-2349 ◽  
Author(s):  
Alan López-López ◽  
Ellen Gelpi ◽  
Diana Maria Lopategui ◽  
Jose M. Vidal-Taboada
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Neurofibrillary Pathology

scholarly journals Non-invasive assessment of Alzheimer’s disease neurofibrillary pathology using 18F-THK5105 PET

Brain ◽  
2014 ◽  
Vol 137 (6) ◽  
pp. 1762-1771 ◽  
Author(s):  
Nobuyuki Okamura ◽  
Shozo Furumoto ◽  
Michelle T. Fodero-Tavoletti ◽  
Rachel S. Mulligan ◽  
Ryuichi Harada ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Pathology ◽  
Non Invasive

scholarly journals Bioinformatics analysis of differentially expressed genes and identification of an miRNA–mRNA network associated with entorhinal cortex and hippocampus in Alzheimer’s disease

Hereditas ◽  
2021 ◽  
Vol 158 (1) ◽  
Author(s):  
Haoming Li ◽  
Linqing Zou ◽  
Jinhong Shi ◽  
Xiao Han
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Differentially Expressed Genes ◽  
Entorhinal Cortex ◽  
Molecular Mechanisms ◽  
Kegg Pathway ◽  
Neurodegenerative Disorder ◽  
Early Stage ◽  
Differentially Expressed ◽  
Hub Genes

Abstract Background Alzheimer’s disease (AD) is a fatal neurodegenerative disorder, and the lesions originate in the entorhinal cortex (EC) and hippocampus (HIP) at the early stage of AD progression. Gaining insight into the molecular mechanisms underlying AD is critical for the diagnosis and treatment of this disorder. Recent discoveries have uncovered the essential roles of microRNAs (miRNAs) in aging and have identified the potential of miRNAs serving as biomarkers in AD diagnosis. Methods We sought to apply bioinformatics tools to investigate microarray profiles and characterize differentially expressed genes (DEGs) in both EC and HIP and identify specific candidate genes and pathways that might be implicated in AD for further analysis. Furthermore, we considered that DEGs might be dysregulated by miRNAs. Therefore, we investigated patients with AD and healthy controls by studying the gene profiling of their brain and blood samples to identify AD-related DEGs, differentially expressed miRNAs (DEmiRNAs), along with gene ontology (GO) analysis, KEGG pathway analysis, and construction of an AD-specific miRNA–mRNA interaction network. Results Our analysis identified 10 key hub genes in the EC and HIP of patients with AD, and these hub genes were focused on energy metabolism, suggesting that metabolic dyshomeostasis contributed to the progression of the early AD pathology. Moreover, after the construction of an miRNA–mRNA network, we identified 9 blood-related DEmiRNAs, which regulated 10 target genes in the KEGG pathway. Conclusions Our findings indicated these DEmiRNAs having the potential to act as diagnostic biomarkers at an early stage of AD.

scholarly journals EAAT2 Expression in the Hippocampus, Subiculum, Entorhinal Cortex and Superior Temporal Gyrus in Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Jason H. Y. Yeung ◽  
Thulani H. Palpagama ◽  
Oliver W. G. Wood ◽  
Clinton Turner ◽  
Henry J. Waldvogel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Excitatory Amino Acid ◽  
Glutamate Uptake ◽  
Expression Patterns ◽  
Superior Temporal Gyrus ◽  
Altered Expression ◽  
And Control ◽  
Transporter Expression

Alzheimer’s disease (AD) is a neuropathological disorder characterized by the presence and accumulation of amyloid-beta plaques and neurofibrillary tangles. Glutamate dysregulation and the concept of glutamatergic excitotoxicity have been frequently described in the pathogenesis of a variety of neurodegenerative disorders and are postulated to play a major role in the progression of AD. In particular, alterations in homeostatic mechanisms, such as glutamate uptake, have been implicated in AD. An association with excitatory amino acid transporter 2 (EAAT2), the main glutamate uptake transporter, dysfunction has also been described. Several animal and few human studies examined EAAT2 expression in multiple brain regions in AD but studies of the hippocampus, the most severely affected brain region, are scarce. Therefore, this study aims to assess alterations in the expression of EAAT2 qualitatively and quantitatively through DAB immunohistochemistry (IHC) and immunofluorescence within the hippocampus, subiculum, entorhinal cortex, and superior temporal gyrus (STG) regions, between human AD and control cases. Although no significant EAAT2 density changes were observed between control and AD cases, there appeared to be increased transporter expression most likely localized to fine astrocytic branches in the neuropil as seen on both DAB IHC and immunofluorescence. Therefore, individual astrocytes are not outlined by EAAT2 staining and are not easily recognizable in the CA1–3 and dentate gyrus regions of AD cases, but the altered expression patterns observed between AD and control hippocampal cases could indicate alterations in glutamate recycling and potentially disturbed glutamatergic homeostasis. In conclusion, no significant EAAT2 density changes were found between control and AD cases, but the observed spatial differences in transporter expression and their functional significance will have to be further explored.

scholarly journals Glutamatergic receptor expression changes in the Alzheimer's disease hippocampus and entorhinal cortex

2021 ◽  
Author(s):  
Jason H. Y. Yeung ◽  
Joshua L. Walby ◽  
Thulani H. Palpagama ◽  
Clinton Turner ◽  
Henry J. Waldvogel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Receptor Expression

Reelin-immunoreactive Cajal-Retzius cells: the entorhinal cortex in normal aging and Alzheimer's disease

2003 ◽  
Vol 106 (4) ◽  
pp. 291-302 ◽  
Author(s):  
Anett Riedel ◽  
Riitta Miettinen ◽  
Jens Stieler ◽  
Mia Mikkonen ◽  
Irina Alafuzoff ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Normal Aging ◽  
Retzius Cells
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