{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T11:51:06Z","timestamp":1781783466208,"version":"3.54.5"},"reference-count":52,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2025,12,4]],"date-time":"2025-12-04T00:00:00Z","timestamp":1764806400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"basic-research project","award":["FWNR-2022-0016"],"award-info":[{"award-number":["FWNR-2022-0016"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Recent evidence suggests that prerequisites for Alzheimer's disease (AD) can form during prenatal and early postnatal development. These prerequisites have been identified to some extent in OXYS rats: a model of the sporadic form of AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Here, we continue to study the role of delayed brain maturation in the development of the AD-like pathology much later in OXYS rats.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We assess synaptic-density changes and gene expression profiles in the prefrontal cortex (PFC) and hippocampus of OXYS and Wistar rats (parental strain; control) between ages \u201cpostnatal day 0\u201d (P0) and P20.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We found that at birth, the synaptic population in the PFC of OXYS rats is half of that in Wistar rats. The proportion of both symmetric (inhibitory) contacts and asymmetric (excitatory) contacts in the hippocampus of OXYS rats at P14 and P20 matched these parameters in Wistar rats at P7 and P14, respectively. The transcriptome analysis of the PFC and hippocampus showed that gene expression profiles related to synapses are different between Wistar and OXYS rats. Next, we identified \u201cage-specific\u201d genes and \u201cbrain region-specific\u201d genes whose changes in the expression can obviously contribute to the specific features of synapse formation in OXYS rats. Finally, analyses of cell-specific (neurons, astrocytes, microglia, oligodendrocytes, and endothelial cells) gene expression suggested that at P3\u2013P20 in the PFC and hippocampus, more than 50% of downregulated genes are associated with glia: key regulators of neural-network functioning.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Collectively, these data indicate a delay in the formation of interneuronal connections and in their efficiency in the OXYS strain.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251396932","type":"journal-article","created":{"date-parts":[[2025,12,4]],"date-time":"2025-12-04T14:45:23Z","timestamp":1764859523000},"page":"685-698","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["The early postnatal synapse assembly and expression profiles of synapse-related genes in a sporadic Alzheimer's disease-like pathology"],"prefix":"10.1177","volume":"109","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5127-5993","authenticated-orcid":false,"given":"Natalia A","family":"Stefanova","sequence":"first","affiliation":[{"name":"Institute of Cytology and Genetics, Novosibirsk, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kseniya Y","family":"Maksimova","sequence":"additional","affiliation":[{"name":"Siberian State Medical University, Tomsk, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mikhail A","family":"Tyumentsev","sequence":"additional","affiliation":[{"name":"Institute of Cytology and Genetics, Novosibirsk, Russia"},{"name":"University of Tennessee Health Science Center, Memphis, TN, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darya V","family":"Telegina","sequence":"additional","affiliation":[{"name":"Institute of Cytology and Genetics, Novosibirsk, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivana I","family":"Khodunova-Zhukovskaia","sequence":"additional","affiliation":[{"name":"Novosibirsk State University, Novosibirsk, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ekaterina A","family":"Rudnitsky","sequence":"additional","affiliation":[{"name":"Ben Gurion University of the Negev, Beer Sheva, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2398-8544","authenticated-orcid":false,"given":"Nataliya G","family":"Kolosova","sequence":"additional","affiliation":[{"name":"Institute of Cytology and Genetics, Novosibirsk, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,12,4]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0379-23.2023"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcdb.2022.05.028"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcdb.2022.07.011"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ntt.2019.106834"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2018.09.040"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2014.03.045"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1542\/peds.2014-3556"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.3390\/nu10091172"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1186\/s13195-018-0422-7"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2022.834661"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41386-021-01137-9"},{"key":"e_1_3_3_13_2","volume-title":"World Alzheimer Report 2016. 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