Cognitive impairment in an animal model of multiple sclerosis and its amelioration by glatiramer acetate
| Autor: | Dekel D. Bar-Lev, Michael Sela, Nofar Schottlender, Michael Tsoory, Ruth Arnon, Rina Aharoni, Raya Eilam |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Encephalomyelitis Autoimmune Experimental Movement Anti-Inflammatory Agents Hippocampus lcsh:Medicine Brain damage Article 03 medical and health sciences Mice 0302 clinical medicine Cognition Medicine Animals Glatiramer acetate lcsh:Science Maze Learning Cognitive deficit Multidisciplinary business.industry Long-term memory Multiple sclerosis Experimental autoimmune encephalomyelitis lcsh:R Glatiramer Acetate medicine.disease Frontal Lobe Mice Inbred C57BL 030104 developmental biology Neuroprotective Agents lcsh:Q medicine.symptom business Neuroscience 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Scientific Reports Scientific Reports, Vol 9, Iss 1, Pp 1-15 (2019) |
| ISSN: | 2045-2322 |
| Popis: | The severe motor impairment in the MS animal model experimental autoimmune encephalomyelitis (EAE) obstructs the assessment of cognitive functions. We developed an experimental system that evaluates memory faculties in EAE-affected mice, irrespective of their motor performance, enabling the assessment of cognitive impairments along the disease duration, the associated brain damage, and the consequences of glatiramer acetate (GA) treatment on these manifestations. The delayed-non-matching to sample (DNMS) T-maze task, testing working and long term memory was adapted and utilized. Following the appearance of clinical manifestations task performances of the EAE-untreated mice drastically declined. Cognitive impairments were associated with disease severity, as indicated by a significant correlation between the T-maze performance and the clinical symptoms in EAE-untreated mice. GA-treatment conserved cognitive functions, so that despite their exhibited mild motor impairments, the treated mice performed similarly to naïve controls. The cognitive deficit of EAE-mice coincided with inflammatory and neurodegenerative damage to the frontal cortex and the hippocampus; these damages were alleviated by GA-treatment. These combined findings indicate that in addition to motor impairment, EAE leads to substantial impairment of cognitive functions, starting at the early stages and increasing with disease aggravation. GA-treatment, conserves cognitive capacities and prevents its disease related deterioration. |
| Databáze: | OpenAIRE |
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