PERFORM Publications

Keyword search (4,163 papers available)

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 MyLo CRISPR-Cas9 Toolkit: A Markerless Yeast Localization and Overexpression CRISPR-Cas9 Toolkit	Bean BDM; Whiteway M; Martin VJJ;	35708612 BIOLOGY
4	Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex	Olajide OJ; Chapman CA;	34144329 PSYCHOLOGY
5	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
6	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
7	Flavanone glycosides inhibit β-site amyloid precursor protein cleaving enzyme 1 and cholinesterase and reduce Aβ aggregation in the amyloidogenic pathway.	Ali MY, Jannat S, Edraki N, Das S, Chang WK, Kim HC, Park SK, Chang MS	31194956 BIOLOGY
8	Amyloid and tau signatures of brain metabolic decline in preclinical Alzheimer's disease.	Pascoal TA, Mathotaarachchi S, Shin M, Park AY, Mohades S, Benedet AL, Kang MS, Massarweh G, Soucy JP, Gauthier S, Rosa-Neto P, Alzheimer’s Disease Neuroimaging Initiative	29396637 PERFORM

Title:	Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.
Authors:	Olajide OJ, Suvanto ME, Chapman CA
Link:	https://www.ncbi.nlm.nih.gov/pubmed/33495355
DOI:	10.1242/bio.056796
Publication:	Biology open
Keywords:	Alzheimer'; s disease; Amyloid beta protein; Apoptosis; Entorhinal cortex; Excitotoxicity; Glia activation; Inflammation; Oxidative stress; Tau;
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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