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

Author(s): Olajide OJ, Suvanto ME, Chapman CA

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 Al...

Article GUID: 33495355
State-Dependent Entrainment of Prefrontal Cortex Local Field Potential Activity Following Patterned Stimulation of the Cerebellar Vermis.

Author(s): Tremblay SA, Chapman CA, Courtemanche R

Front Syst Neurosci. 2019;13:60 Authors: Tremblay SA, Chapman CA, Courtemanche R

Article GUID: 31736718
Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum.

Author(s): Sparks DW, Chapman CA

J Neurophysiol. 2016 08 01;116(2):658-70 Authors: Sparks DW, Chapman CA

Article GUID: 27146979
Gap Junction Modulation of Low-Frequency Oscillations in the Cerebellar Granule Cell Layer.

Author(s): Robinson JC, Chapman CA, Courtemanche R

Cerebellum. 2017 08;16(4):802-811 Authors: Robinson JC, Chapman CA, Courtemanche R

Article GUID: 28421552
Exposure to cues associated with palatable food reward results in a dopamine D₂ receptor-dependent suppression of evoked synaptic responses in the entorhinal cortex.

Author(s): Hutter JA, Chapman CA

Behav Brain Funct. 2013 Oct 04;9:37 Authors: Hutter JA, Chapman CA

Article GUID: 24093833
Dopaminergic enhancement of excitatory synaptic transmission in layer II entorhinal neurons is dependent on D₁-like receptor-mediated signaling.

Author(s): Glovaci I, Caruana DA, Chapman CA

Neuroscience. 2014 Jan 31;258:74-83 Authors: Glovaci I, Caruana DA, Chapman CA

Article GUID: 24220689
Diurnal influences on electrophysiological oscillations and coupling in the dorsal striatum and cerebellar cortex of the anesthetized rat.

Author(s): Frederick A, Bourget-Murray J, Chapman CA, Amir S, Courtemanche R

Front Syst Neurosci. 2014;8:145 Authors: Frederick A, Bourget-Murray J, Chapman CA, Amir S, Courtemanche R

Article GUID: 25309348
Activation of Phosphatidylinositol-Linked Dopamine Receptors Induces a Facilitation of Glutamate-Mediated Synaptic Transmission in the Lateral Entorhinal Cortex.

Author(s): Glovaci I, Chapman CA

PLoS One. 2015;10(7):e0131948 Authors: Glovaci I, Chapman CA

Article GUID: 26133167
Optogenetic Activation of the Infralimbic Cortex Suppresses the Return of Appetitive Pavlovian-Conditioned Responding Following Extinction.

Author(s): Villaruel FR, Lacroix F, Sanio C, Sparks DW, Chapman CA, Chaudhri N

Cereb Cortex. 2018 Dec 01;28(12):4210-4221 Authors: Villaruel FR, Lacroix F, Sanio C, Sparks DW, Chapman CA, Chaudhri N

Article GUID: 29045570
Dopamine suppresses persistent firing in layer III lateral entorhinal cortex neurons.

Author(s): Batallán-Burrowes AA, Chapman CA

Neurosci Lett. 2018 05 01;674:70-74 Authors: Batallán-Burrowes AA, Chapman CA

Article GUID: 29524644
The role of the paraventricular nucleus of the thalamus in the augmentation of heroin seeking induced by chronic food restriction.

Author(s): Chisholm A, Iannuzzi J, Rizzo D, Gonzalez N, Fortin É, Bumbu A, Batallán Burrowes AA, Chapman CA, Shalev U

Addict Biol. 2019 Jan 09;: Authors: Chisholm A, Iannuzzi J, Rizzo D, Gonzalez N, Fortin É, Bumbu A, Batallán Burrowes AA, Chapman CA, Shalev U

Article GUID: 30623532
Serotonin 5-HT1A Receptor-Mediated Reduction of Excitatory Synaptic Transmission in Layers II/III of the Parasubiculum.

Author(s): Carter F, Chapman CA

Neuroscience. 2019 May 15;406:325-332 Authors: Carter F, Chapman CA

Article GUID: 30902681
Dopamine induces release of calcium from internal stores in layer II lateral entorhinal cortex fan cells.

Author(s): Glovaci I, Chapman CA

Cell Calcium. 2019 Apr 10;80:103-111 Authors: Glovaci I, Chapman CA

Article GUID: 30999216
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
Category:Biol Open
PMID:33495355
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]