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Title Authors PubMed ID
1 Longitudinal relationships among cerebrospinal fluid biomarkers, cerebral blood flow, and grey matter volume in individuals with a familial history of Alzheimer s disease Sanami S; Intzandt B; Huck J; Villeneuve S; Iturria-Medina Y; Gauthier CJ; Prevent-Ad Research Group None; 40347524
CONCORDIA
2 Sleep spindles and slow oscillations predict cognition and biomarkers of neurodegeneration in mild to moderate Alzheimer's disease Páez A; Gillman SO; Dogaheh SB; Carnes A; Dakterzada F; Barbé F; Dang-Vu TT; Ripoll GP; 39878233
CONCORDIA
3 The β2-adrenergic biased agonist nebivolol inhibits the development of Th17 and the response of memory Th17 cells in an NF-κB-dependent manner Hajiaghayi M; Gholizadeh F; Han E; Little SR; Rahbari N; Ardila I; Lopez Naranjo C; Tehranimeh K; Shih SCC; Darlington PJ; 39445009
BIOLOGY
4 Effects of early midlife ovarian removal on sleep: Polysomnography-measured cortical arousal, homeostatic drive, and spindle characteristics Brown A; Gervais NJ; Gravelsins L; O' Byrne J; Calvo N; Ramana S; Shao Z; Bernardini M; Jacobson M; Rajah MN; Einstein G; 39178647
HKAP
5 The β2-adrenergic receptor agonist terbutaline upregulates T helper-17 cells in a protein kinase A-dependent manner Carvajal Gonczi CM; Hajiaghayi M; Gholizadeh F; Xavier Soares MA; Touma F; Lopez Naranjo C; Rios AJ; Pozzebon C; Daigneault T; Burchell-Reyes K; Darlington PJ; 37438188
PERFORM
6 Cross-collection latent Beta-Liouville allocation model training with privacy protection and applications Luo Z; Amayri M; Fan W; Bouguila N; 36685642
ENCS
7 Estrogen receptors observed at extranuclear neuronal sites and in glia in the nucleus accumbens core and shell of the female rat: Evidence for localization to catecholaminergic and GABAergic neurons Almey A; Milner TA; Brake WG; 35397175
CSBN
8 Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex Olajide OJ; Chapman CA; 34144329
PSYCHOLOGY
9 Data-driven beamforming technique to attenuate ballistocardiogram artefacts in electroencephalography-functional magnetic resonance imaging without detecting cardiac pulses in electrocardiography recordings Uji M; Cross N; Pomares FB; Perrault AA; Jegou A; Nguyen A; Aydin U; Lina JM; Dang-Vu TT; Grova C; 34101939
PERFORM
10 How cerebral cortex protects itself from interictal spikes: The alpha/beta inhibition mechanism Pellegrino G; Hedrich T; Sziklas V; Lina JM; Grova C; Kobayashi E; 34002916
PERFORM
11 Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease. Olajide OJ, Suvanto ME, Chapman CA 33495355
PSYCHOLOGY
12 Topographical distribution of Aβ predicts progression to dementia in Aβ positive mild cognitive impairment Pascoal TA, Therriault J, Mathotaarachchi S, Kang MS, Shin M, Benedet AL, Chamoun M, Tissot C, Lussier F, Mohaddes S, Soucy JP, Massarweh G, Gauthier S, Rosa-Neto P, 32582834
PERFORM
13 Comparison of underivatized silica and zwitterionic sulfobetaine hydrophilic interaction liquid chromatography stationary phases for global metabolomics of human plasma Sonnenberg RA; Naz S; Cougnaud L; Vuckovic D; 31439439
CHEMBIOCHEM
14 Reciprocal modulation of helper Th1 and Th17 cells by the β2-adrenergic receptor agonist drug terbutaline. Carvajal Gonczi CM, Tabatabaei Shafiei M, East A, Martire E, Maurice-Ventouris MHI, Darlington PJ 28710773
PERFORM

 

Title:Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.
Authors:Olajide OJSuvanto MEChapman CA
Link:https://www.ncbi.nlm.nih.gov/pubmed/33495355
DOI:10.1242/bio.056796
Publication:Biology open
Keywords:Alzheimer's diseaseAmyloid beta proteinApoptosisEntorhinal cortexExcitotoxicityGlia activationInflammationOxidative stressTau
PMID:33495355 Category:Biol Open Date Added:2021-01-27
Dept Affiliation: PSYCHOLOGY
1 Division of Neurobiology, Department of Anatomy, University of Ilorin, Ilorin, Nigeria, PMB 1515 olajide.oj@unilorin.edu.ng joseph.olajide@concordia.ca andrew.chapman@concordia.ca.
2 Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada H4B 1R6.
3 Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada H4B 1R6 olajide.oj@unilorin.edu.ng joseph.olajide@concordia.ca andrew.chapman@concordia.ca.

Description:

Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.

Biol Open. 2021 Jan 25; 10(1):

Authors: Olajide OJ, Suvanto ME, Chapman CA

Abstract

The entorhinal cortex (EC) is a vital component of the medial temporal lobe, and its contributions to cognitive processes and memory formation are supported through its extensive interconnections with the hippocampal formation. During the pathogenesis of Alzheimer's disease (AD), many of the earliest degenerative changes are seen within the EC. Neurodegeneration in the EC and hippocampus during AD has been clearly linked to impairments in memory and cognitive function, and a growing body of evidence indicates that molecular and functional neurodegeneration within the EC may play a primary role in cognitive decline in the early phases of AD. Defining the mechanisms underlying molecular neurodegeneration in the EC is crucial to determining its contributions to the pathogenesis of AD. Surprisingly few studies have focused on understanding the mechanisms of molecular neurodegeneration and selective vulnerability within the EC. However, there have been advancements indicating that early dysregulation of cellular and molecular signaling pathways in the EC involve neurodegenerative cascades including oxidative stress, neuroinflammation, glia activation, stress kinases activation, and neuronal loss. Dysfunction within the EC can impact the function of the hippocampus, which relies on entorhinal inputs, and further degeneration within the hippocampus can compound this effect, leading to severe cognitive disruption. This review assesses the molecular and cellular mechanisms underlying early degeneration in the EC during AD. These mechanisms may underlie the selective vulnerability of neuronal subpopulations in this brain region to the disease development and contribute both directly and indirectly to cognitive loss.This paper has an associated Future Leader to Watch interview with the first author of the article.

PMID: 33495355 [PubMed - in process]





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