PERFORM Publications

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Title		Authors	PubMed ID
1	Dopamine inhibits excitatory synaptic responses in layer I of the rat parasubiculum	Carter F; Hobishi H; Chapman CA;	40818632 PSYCHOLOGY
2	Progesterone and allopregnanolone facilitate excitatory synaptic transmission in the infralimbic cortex via activation of membrane progesterone receptors	Rahaei N; Buynack LM; Kires L; Movasseghi Y; Chapman CA;	39722289 PSYCHOLOGY
3	Reduced 17β-estradiol following ovariectomy induces mitochondrial dysfunction and degradation of synaptic proteins in the entorhinal cortex	Olajide OJ; Batallán Burrowes AA; da Silva IF; Bergdahl A; Chapman CA;	39617168 HKAP
4	17β-Estradiol reduces inhibitory synaptic currents in entorhinal cortex neurons through G protein-coupled estrogen receptor-1 activation of extracellular signal-regulated kinase	Batallán Burrowes AA; Moisan É; Garrone A; Buynack LM; Chapman CA;	39150316 PSYCHOLOGY
5	Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex	Olajide OJ; La Rue C; Bergdahl A; Chapman CA;	36275011 HKAP
6	Ovariectomy reduces cholinergic modulation of excitatory synaptic transmission in the rat entorhinal cortex	Batallán Burrowes AA; Olajide OJ; Iasenza IA; Shams WM; Carter F; Chapman CA;	35939438 CSBN
7	G protein-coupled estrogen receptor-1 enhances excitatory synaptic responses in the entorhinal cortex	Batallán Burrowes AA; Sundarakrishnan A; Bouhour C; Chapman CA;	34399010 PSYCHOLOGY
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	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
10	State-Dependent Entrainment of Prefrontal Cortex Local Field Potential Activity Following Patterned Stimulation of the Cerebellar Vermis.	Tremblay SA, Chapman CA, Courtemanche R	31736718 HKAP
11	Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum.	Sparks DW, Chapman CA	27146979 PSYCHOLOGY
12	Gap Junction Modulation of Low-Frequency Oscillations in the Cerebellar Granule Cell Layer.	Robinson JC, Chapman CA, Courtemanche R	28421552 HKAP
13	Exposure to cues associated with palatable food reward results in a dopamine D₂ receptor-dependent suppression of evoked synaptic responses in the entorhinal cortex.	Hutter JA, Chapman CA	24093833 CSBN
14	Dopaminergic enhancement of excitatory synaptic transmission in layer II entorhinal neurons is dependent on D₁-like receptor-mediated signaling.	Glovaci I, Caruana DA, Chapman CA	24220689 PSYCHOLOGY
15	Diurnal influences on electrophysiological oscillations and coupling in the dorsal striatum and cerebellar cortex of the anesthetized rat.	Frederick A, Bourget-Murray J, Chapman CA, Amir S, Courtemanche R	25309348 BIOLOGY
16	Activation of Phosphatidylinositol-Linked Dopamine Receptors Induces a Facilitation of Glutamate-Mediated Synaptic Transmission in the Lateral Entorhinal Cortex.	Glovaci I, Chapman CA	26133167 PSYCHOLOGY
17	Optogenetic Activation of the Infralimbic Cortex Suppresses the Return of Appetitive Pavlovian-Conditioned Responding Following Extinction.	Villaruel FR, Lacroix F, Sanio C, Sparks DW, Chapman CA, Chaudhri N	29045570 PSYCHOLOGY
18	Dopamine suppresses persistent firing in layer III lateral entorhinal cortex neurons.	Batallán-Burrowes AA, Chapman CA	29524644 PSYCHOLOGY
19	The role of the paraventricular nucleus of the thalamus in the augmentation of heroin seeking induced by chronic food restriction.	Chisholm A, Iannuzzi J, Rizzo D, Gonzalez N, Fortin É, Bumbu A, Batallán Burrowes AA, Chapman CA, Shalev U	30623532 CSBN
20	Serotonin 5-HT1A Receptor-Mediated Reduction of Excitatory Synaptic Transmission in Layers II/III of the Parasubiculum.	Carter F, Chapman CA	30902681 PSYCHOLOGY
21	Dopamine induces release of calcium from internal stores in layer II lateral entorhinal cortex fan cells.	Glovaci I, Chapman CA	30999216 PSYCHOLOGY

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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