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Neuron-to-Neuron Transmission of Neurodegenerative Pathology
Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics. Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Neuroscience. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Neuroscience. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Geriatric Medicine in Linköping.
2013 (English)In: The Neuroscientist, ISSN 1073-8584, E-ISSN 1089-4098, Vol. 19, no 6, 560-566 p.Article, review/survey (Refereed) Published
Abstract [en]

One of the hallmarks of neurodegenerative dementia diseases is the progressive loss of mental functions and the ability to manage activities of daily life. This progression is caused by the spread of the disease to more and more brain areas via anatomical connections. The pathophysiological process responsible for this spread of disease has long been sought after. There has been an increased understanding that the driving force of these neurodegenerative diseases could be the small, soluble intraneuronal accumulations of neurodegenerative proteins rather than the large, extracellular accumulations. Recently we have shown that the mechanism of spread of Alzheimer's disease most likely depends on the neuron-to-neuron spread of such soluble intraneuronal accumulations of -amyloid through neuritic connections. Similar transmissions have been shown for several other neurodegenerative proteins but little is known about the cellular mechanisms and about any potential strategies that might stop this spread. Resolving these questions requires good cellular models. We have established a unique model of synaptic transmission between human neuronal-like cells, something that has previously been difficult to target. This opens the possibility of developing potential inhibitors of progression of these devastating diseases.

Place, publisher, year, edition, pages
Sage Publications, 2013. Vol. 19, no 6, 560-566 p.
Keyword [en]
Alzheimer’s disease, neurodegeneration, β-amyloid, transmission, prion, cellular models
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:liu:diva-95927DOI: 10.1177/1073858413494270ISI: 000326653000007OAI: oai:DiVA.org:liu-95927DiVA: diva2:639922
Available from: 2013-08-11 Created: 2013-08-11 Last updated: 2017-12-06

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Hallbeck, MartinNath, SangeetaMarcusson, Jan

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Hallbeck, MartinNath, SangeetaMarcusson, Jan
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Department of Clinical Pathology and Clinical GeneticsDivision of Inflammation MedicineFaculty of Health SciencesDivision of NeuroscienceDepartment of Geriatric Medicine in Linköping
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The Neuroscientist
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