scholarly journals Hippocampal Volume and Entorhinal Cortex Thickness in Alzheimer’s Disease

2022 ◽  
Vol 16 (1) ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Hippocampal Volume

P3-031: THE CRITICAL PATH FOR ALZHEIMER'S DISEASE: HIPPOCAMPAL VOLUME AS AN ENRICHMENT BIOMARKER IN TRIALS OF PATIENTS WITH MILD COGNITIVE IMPAIRMENT

2006 ◽  
Vol 14 (7S_Part_20) ◽  
pp. P1076-P1076
Author(s):  
Daniela J. Conrado ◽  
Timothy Nicholas ◽  
Jackson Burton ◽  
Stephen P. Arnerić ◽  
Danny Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Critical Path ◽  
Hippocampal Volume

scholarly journals Circulating biomarkers of immunity and inflammation, risk of Alzheimer’s disease, and hippocampal volume: a Mendelian randomization study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lana Fani ◽  
Marios K. Georgakis ◽  
M. Arfan Ikram ◽  
M. Kamran Ikram ◽  
Rainer Malik ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mendelian Randomization ◽  
Hippocampal Volume ◽  
Cd4 Count ◽  
European Ancestry ◽  
Monocyte Count ◽  
Circulating Biomarkers ◽  
Lymphocyte Ratio ◽  
Immune Biomarkers

AbstractThe aim of this study was to explore the association between genetically predicted circulating levels of immunity and inflammation, and the risk of Alzheimer’s disease (AD) and hippocampal volume, by conducting a two-sample Mendelian Randomization Study. We identified 12 markers of immune cells and derived ratios (platelet count, eosinophil count, neutrophil count, basophil count, monocyte count, lymphocyte count, platelet-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, CD4 count, CD8 count, CD4-to-CD8 ratio, and CD56) and 5 signaling molecules (IL-6, fibrinogen, CRP, and Lp-PLA2 activity and mass) as primary exposures of interest. Other genetically available immune biomarkers with a weaker a priori link to AD were considered secondary exposures. Associations with AD were evaluated in The International Genomics of Alzheimer’s Project (IGAP) GWAS dataset (21,982 cases; 41,944 controls of European ancestry). For hippocampal volume, we extracted data from a GWAS meta-analysis on 33,536 participants of European ancestry. None of the primary or secondary exposures showed statistically significant associations with AD or with hippocampal volume following P-value correction for multiple comparisons using false discovery rate < 5% (Q-value < 0.05). CD4 count showed the strongest suggestive association with AD (odds ratio 1.32, P < 0.01, Q > 0.05). There was evidence for heterogeneity in the MR inverse variance-weighted meta-analyses as measured by Cochran Q, and weighted median and weighted mode for multiple exposures. Further cluster analyses did not reveal clusters of variants that could influence the risk factor in distinct ways. This study suggests that genetically predicted circulating biomarkers of immunity and inflammation are not associated with AD risk or hippocampal volume. Future studies should assess competing risk, explore in more depth the role of adaptive immunity in AD, in particular T cells and the CD4 subtype, and confirm these findings in other ethnicities.

Elevated basal cortisol level predicts lower hippocampal volume and cognitive decline in Alzheimer’s disease

2009 ◽  
Vol 16 (10) ◽  
pp. 1283-1286 ◽  
Author(s):  
Chi-Wei Huang ◽  
Chun-Chung Lui ◽  
Weng-Neng Chang ◽  
Cheng-Hsien Lu ◽  
Ya-Ling Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Cortisol Level ◽  
Hippocampal Volume ◽  
Basal Cortisol ◽  
Basal Cortisol Level

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

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 Herpes simplex virus, early neuroimaging markers and incidence of Alzheimer’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Morgane Linard ◽  
Marion Baillet ◽  
Luc Letenneur ◽  
Isabelle Garrigue ◽  
Gwenaëlle Catheline ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Diffusion Tensor ◽  
Hippocampal Volume ◽  
Potential Interaction ◽  
Increased Risk ◽  
Simplex Virus ◽  
Igg Level

AbstractWhile previous studies suggest the implication of herpes simplex virus (HSV) in the onset of Alzheimer’s disease (AD), no study has investigated its association with early neuroimaging markers of AD. In the Three-City and the AMI cohorts, the associations between HSV infection and (i) hippocampal volume (n = 349), (ii) white matter alterations in the parahippocampal cingulum and fornix using diffusion tensor imaging (n = 260), and (iii) incidence of AD (n = 1599) were assessed according to APOE4 status. Regardless of APOE4 status, infected subjects presented (i) significantly more microstructural alterations of the parahippocampal cingulum and fornix, (ii) lower hippocampal volumes only when their anti-HSV IgG level was in the highest tercile—reflecting possibly more frequent reactivations of the virus (p = 0.03 for subjects with a high anti-HSV IgG level while there was no association for all infected subjects, p = 0.19), and (iii) had no increased risk of developing AD. Nevertheless, among APOE4 carriers, infected subjects presented lower hippocampal volumes, although not significant (p = 0.09), and a two or three times higher risk of developing AD (adjusted Hazard ratio (aHR) = 2.72 [1.07–6.91] p = 0.04 for infected subjects and aHR = 3.87 [1.45–10.28] p = 0.007 for infected subjects with an anti-HSV IgG level in the highest tercile) while no association was found among APOE4 noncarriers. Our findings support an association between HSV infection and AD and a potential interaction between HSV status and APOE4. This reinforces the need to further investigate the infectious hypothesis of AD, especially the associated susceptibility factors and the possibility of preventive treatments.

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.

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