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Alzheimer Disease: HELP
Articles by Benjamin Kolisnyk
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, Benjamin Kolisnyk wrote the following 4 articles about Alzheimer Disease.
 
+ Citations + Abstracts
1 Article MouseBytes, an open-access high-throughput pipeline and database for rodent touchscreen-based cognitive assessment. 2019

Beraldo, Flavio H / Palmer, Daniel / Memar, Sara / Wasserman, David I / Lee, Wai-Jane V / Liang, Shuai / Creighton, Samantha D / Kolisnyk, Benjamin / Cowan, Matthew F / Mels, Justin / Masood, Talal S / Fodor, Chris / Al-Onaizi, Mohammed A / Bartha, Robert / Gee, Tom / Saksida, Lisa M / Bussey, Timothy J / Strother, Stephen S / Prado, Vania F / Winters, Boyer D / Prado, Marco Am. ·Robarts Research Institute, The University of Western Ontario, Ontario, Canada. · Graduate Program in Neuroscience, The University of Western Ontario, Ontario, Canada. · Department of Physiology and Pharmacology, The University of Western Ontario, Ontario, Canada. · Department of Psychology and Neuroscience Program, University of Guelph, Guelph, Canada. · Rotman Research Institute, Baycrest Hospital, Toronto, Canada. · Department of Anatomy and Cell Biology, The University of Western Ontario, Ontario, Canada. · Department of Medical Biophysics, The University of Western Ontario, London, Canada. · Brain and Mind Institute, The University of Western Ontario, Ontario, Canada. · Department of Medical Biophysics, University of Toronto, Toronto, Canada. ·Elife · Pubmed #31825307.

ABSTRACT: Open Science has changed research by making data accessible and shareable, contributing to replicability to accelerate and disseminate knowledge. However, for rodent cognitive studies the availability of tools to share and disseminate data is scarce. Automated touchscreen-based tests enable systematic cognitive assessment with easily standardised outputs that can facilitate data dissemination. Here we present an integration of touchscreen cognitive testing with an open-access database public repository (mousebytes.ca), as well as a Web platform for knowledge dissemination (https://touchscreencognition.org). We complement these resources with the largest dataset of age-dependent high-level cognitive assessment of mouse models of Alzheimer's disease, expanding knowledge of affected cognitive domains from male and female mice of three strains. We envision that these new platforms will enhance sharing of protocols, data availability and transparency, allowing meta-analysis and reuse of mouse cognitive data to increase the replicability/reproducibility of datasets.

2 Article Cholinergic Surveillance over Hippocampal RNA Metabolism and Alzheimer's-Like Pathology. 2017

Kolisnyk, Benjamin / Al-Onaizi, Mohammed / Soreq, Lilach / Barbash, Shahar / Bekenstein, Uriya / Haberman, Nejc / Hanin, Geula / Kish, Maxine T / Souza da Silva, Jussemara / Fahnestock, Margaret / Ule, Jernej / Soreq, Hermona / Prado, Vania F / Prado, Marco A M. ·Robarts Research Institute. · Graduate Program in Neuroscience. · Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8. · Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK. · The Edmond and Lily Safra Center for Brain Science and The Silberman Institute of Life Sciences, The Edmond J Safra Campus, The Hebrew University of Jerusalem, Jerusalem 91904, Israel. · Department of Physiology and Pharmacology. · Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, CanadaL8S 4K1. ·Cereb Cortex · Pubmed #27312991.

ABSTRACT: The relationship between long-term cholinergic dysfunction and risk of developing dementia is poorly understood. Here we used mice with deletion of the vesicular acetylcholine transporter (VAChT) in the forebrain to model cholinergic abnormalities observed in dementia. Whole-genome RNA sequencing of hippocampal samples revealed that cholinergic failure causes changes in RNA metabolism. Remarkably, key transcripts related to Alzheimer's disease are affected. BACE1, for instance, shows abnormal splicing caused by decreased expression of the splicing regulator hnRNPA2/B1. Resulting BACE1 overexpression leads to increased APP processing and accumulation of soluble Aβ1-42. This is accompanied by age-related increases in GSK3 activation, tau hyperphosphorylation, caspase-3 activation, decreased synaptic markers, increased neuronal death, and deteriorating cognition. Pharmacological inhibition of GSK3 hyperactivation reversed deficits in synaptic markers and tau hyperphosphorylation induced by cholinergic dysfunction, indicating a key role for GSK3 in some of these pathological changes. Interestingly, in human brains there was a high correlation between decreased levels of VAChT and hnRNPA2/B1 levels with increased tau hyperphosphorylation. These results suggest that changes in RNA processing caused by cholinergic loss can facilitate Alzheimer's-like pathology in mice, providing a mechanism by which decreased cholinergic tone may increase risk of dementia.

3 Article Regulation of Cognitive Processing by Hippocampal Cholinergic Tone. 2017

Al-Onaizi, Mohammed A / Parfitt, Gustavo M / Kolisnyk, Benjamin / Law, Clayton S H / Guzman, Monica S / Barros, Daniela Martí / Leung, L Stan / Prado, Marco A M / Prado, Vania F. ·Robarts Research Institute. · Department of Anatomy and Cell Biology. · Programa de Pós-graduação em Ciências Fisiológicas, Fisiologia Animal Comparada, Laboratório de Neurociências (FURG), Brazil. · Graduate Program in Neuroscience and. · Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, CanadaN6A5K8. · Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8. ·Cereb Cortex · Pubmed #26803167.

ABSTRACT: Cholinergic dysfunction has been associated with cognitive abnormalities in a variety of neurodegenerative and neuropsychiatric diseases. Here we tested how information processing is regulated by cholinergic tone in genetically modified mice targeting the vesicular acetylcholine transporter (VAChT), a protein required for acetylcholine release. We measured long-term potentiation of Schaffer collateral-CA1 synapses in vivo and assessed information processing by using a mouse touchscreen version of paired associates learning task (PAL). Acquisition of information in the mouse PAL task correlated to levels of hippocampal VAChT, suggesting a critical role for cholinergic tone. Accordingly, synaptic plasticity in the hippocampus in vivo was disturbed, but not completely abolished, by decreased hippocampal cholinergic signaling. Disrupted forebrain cholinergic signaling also affected working memory, a result reproduced by selectively decreasing VAChT in the hippocampus. In contrast, spatial memory was relatively preserved, whereas reversal spatial memory was sensitive to decreased hippocampal cholinergic signaling. This work provides a refined roadmap of how synaptically secreted acetylcholine influences distinct behaviors and suggests that distinct forms of cognitive processing may be regulated in different ways by cholinergic activity.

4 Article Cholinergic Regulation of hnRNPA2/B1 Translation by M1 Muscarinic Receptors. 2016

Kolisnyk, Benjamin / Al-Onaizi, Mohammed A / Xu, Jason / Parfitt, Gustavo M / Ostapchenko, Valeriy G / Hanin, Geula / Soreq, Hermona / Prado, Marco A M / Prado, Vania F. ·Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8, and Graduate Program in Neuroscience. · Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8, and Anatomy and Cell Biology. · Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8, and. · Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8, and Departments of Physiology and Pharmacology and. · The Edmond and Lily Safra Center for Brain Sciences, and The Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel 91904. · Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada N6A5K8, and Graduate Program in Neuroscience, Departments of Physiology and Pharmacology and Anatomy and Cell Biology, mprado@robarts.ca vprado@robarts.ca. ·J Neurosci · Pubmed #27277805.

ABSTRACT: SIGNIFICANCE STATEMENT: In Alzheimer's disease, degeneration of basal forebrain cholinergic neurons is an early event. These neurons communicate with target cells and regulate their long-term activity by poorly understood mechanisms. Recently, the splicing factor hnRNPA2/B, which is decreased in Alzheimer's disease, was implicated as a potential mediator of long-term cholinergic regulation. Here, we demonstrate a mechanism by which cholinergic signaling controls the translation of hnRNPA2/B1 mRNA by activation of M1 muscarinic type receptors. Loss of cholinergic activity can have profound effects in target cells by modulating hnRNPA2/B1 levels.