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There is, however, a growing body of evidence that synaptic dysfunction may be crucial for the development of the most common (sporadic) form of\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    . The applicability of melatonin (mainly produced by the pineal gland) to the treatment of\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    is actively evaluated, but usually, such studies are based on animal models of early\u2010onset\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    , which is responsible for only ~5% of\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    cases. We have shown previously that in\n                    <jats:styled-content style=\"fixed-case\">OXYS<\/jats:styled-content>\n                    rats (an established model of sporadic\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    ), accumulation of toxic forms of A\n                    <jats:italic>\u03b2<\/jats:italic>\n                    in the brain occurs later than does the development of signs of neurodegenerative changes and synaptic failure. In this regard, recently, we uncovered beneficial neuroprotective effects of melatonin (prophylactic dietary supplementation) in\n                    <jats:styled-content style=\"fixed-case\">OXYS<\/jats:styled-content>\n                    rats. Our aim here was to evaluate, starting at the age of active progression of\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    \u2010like pathology in\n                    <jats:styled-content style=\"fixed-case\">OXYS<\/jats:styled-content>\n                    rats, the effects of long\u2010term oral administration of melatonin on the structure of synapses and on neuronal and glial cells of the hippocampus. Melatonin significantly increased hippocampal synaptic density and the number of excitatory synapses, decreased the number of inhibitory synapses, and upregulated pre\u2010 and postsynaptic proteins (synapsin I and\n                    <jats:styled-content style=\"fixed-case\">PSD<\/jats:styled-content>\n                    \u201095, respectively). Furthermore, melatonin improved the ultrastructure of neuronal and glial cells and reduced glial density. Based on our past and present results, the repair of neuroplasticity by melatonin is a promising strategy against\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/jpi.12248","type":"journal-article","created":{"date-parts":[[2015,5,19]],"date-time":"2015-05-19T08:21:45Z","timestamp":1432023705000},"page":"163-177","source":"Crossref","is-referenced-by-count":78,"title":["Melatonin attenuates impairments of structural hippocampal neuroplasticity in\n                    <scp>OXYS<\/scp>\n                    rats during active progression of\n                    <scp>A<\/scp>\n                    lzheimer's disease\u2010like pathology"],"prefix":"10.1111","volume":"59","author":[{"given":"Natalia A.","family":"Stefanova","sequence":"first","affiliation":[{"name":"Institute of Cytology and Genetics Novosibirsk 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