{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T17:40:08Z","timestamp":1793814008407,"version":"4.6.1"},"reference-count":92,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T00:00:00Z","timestamp":1764115200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T00:00:00Z","timestamp":1764115200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Agencia Espa\u00f1ola de Investigacion","award":["PID2021-125875OB-I00"],"award-info":[{"award-number":["PID2021-125875OB-I00"]}]},{"DOI":"10.13039\/501100011698","name":"Junta de Comunidades de Castilla-La Mancha","doi-asserted-by":"publisher","award":["SBPLY\/24\/180225\/000007"],"award-info":[{"award-number":["SBPLY\/24\/180225\/000007"]}],"id":[{"id":"10.13039\/501100011698","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Agencia Espa\u00f1ola de Investigaci\u00f3n","award":["PID2024-155887OB-I00"],"award-info":[{"award-number":["PID2024-155887OB-I00"]}]},{"DOI":"10.13039\/501100007480","name":"Universidad de Castilla-La Mancha","doi-asserted-by":"publisher","award":["2025-GRIN-38362"],"award-info":[{"award-number":["2025-GRIN-38362"]}],"id":[{"id":"10.13039\/501100007480","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["1059002414"],"award-info":[{"award-number":["1059002414"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"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>\n                      Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 (R-type) channels mediate calcium signals involved in neuronal excitability, synaptic plasticity, and neurotransmitter release in the hippocampus. However, there is currently no information about their potential changes in Alzheimer's disease (AD).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      This study aims to analyze the protein levels, expression, and subcellular localization of Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 channels in the hippocampus of 5xFAD mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We employed histoblot, western blot, qRT-PCR, and immunoelectron microscopy techniques.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Using the histoblot technique, we observed that the protein content of Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 in female 5xFAD mice was downregulated in the hippocampus and caudate putamen at 5 months, with more pronounced downregulation at 10 months that also affected the septum. The hippocampus was the most affected region, where Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 immunodetection was significantly decreased in a few dendritic layers at 5 months, but this reduction extended to all layers and subregions by 10 months, demonstrating age- and laminar-dependent changes. The pattern in females differed from that seen in males and remained unchanged in APP\/PS1 and P301S mice. Immunoelectron microscopy of the hippocampus showed Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 in apical and oblique dendrites of CA1 pyramidal cells, with a significantly higher presence in dendritic spines. Quantification revealed a significant decrease in the density of Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 in oblique dendrites and dendritic spines of CA1 pyramidal cells, whereas apical dendrites and presynaptic compartments were unaffected in 5xFAD mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Overall, this downregulation in postsynaptic Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.3 channels could impact neural circuit activity and contribute to the cognitive deficits observed in 5xFAD mice.\n                    <\/jats:p>\n                  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