{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T20:08:07Z","timestamp":1785182887684,"version":"3.55.0"},"reference-count":202,"publisher":"SAGE Publications","issue":"12","license":[{"start":{"date-parts":[[2018,9,14]],"date-time":"2018-09-14T00:00:00Z","timestamp":1536883200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>\n                      Numerous cellular processes and signaling mechanisms have been identified that contribute to Alzheimer's disease (AD) pathology; however, a comprehensive or unifying pathway that binds together the major disease features remains elusive. As an upstream mechanism, altered calcium (Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ) signaling is a common driving force for many pathophysiological events that emerge during normal aging and development of neurodegenerative disease.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Advances:<\/jats:title>\n                    <jats:p>\n                      Over the previous three decades, accumulated evidence has validated the concept that intracellular Ca\n                      <jats:sup>2+<\/jats:sup>\n                      dysregulation is centrally involved in AD pathogenesis, including the aggregation of pathogenic \u03b2-amyloid (A\u03b2) and phospho-\u03c4 species, synapse loss and dysfunction, cognitive impairment, and neurotoxicity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Critical Issues:<\/jats:title>\n                    <jats:p>\n                      Although neuronal Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signaling within the cytosol and endoplasmic reticulum (ER) has been well studied, other critical central nervous system-resident cell types affected by aberrant Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signaling, such as astrocytes and microglia, have not been considered as thoroughly. In addition, certain intracellular Ca\n                      <jats:sup>2+<\/jats:sup>\n                      -harboring organelles have been well studied, such as the ER and mitochondria; however other critical Ca\n                      <jats:sup>2+<\/jats:sup>\n                      -regulated organelles, such as lysosomes and autophagosomes, have only more recently been investigated. In this review, we examine Ca\n                      <jats:sup>2+<\/jats:sup>\n                      dysregulation in microglia and astrocytes, as well as key intracellular organelles important for cellular maintenance and protein handling. Ca\n                      <jats:sup>2+<\/jats:sup>\n                      dysregulation within these non-neuronal cells and organelles is hypothesized to disrupt the effective clearance of misaggregated proteins and cellular signaling pathways needed for memory networks.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Future Directions:<\/jats:title>\n                    <jats:p>\n                      Overall, we aim to explore how these disrupted mechanisms could be involved in AD pathology and consider their role as potential therapeutic targets.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      29, 1158\u20131175.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2017.7266","type":"journal-article","created":{"date-parts":[[2018,3,29]],"date-time":"2018-03-29T11:42:53Z","timestamp":1522323773000},"page":"1158-1175","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":41,"title":["Calcium Signaling Deficits in Glia and Autophagic Pathways Contributing to Neurodegenerative Disease"],"prefix":"10.1177","volume":"29","author":[{"given":"Sarah","family":"Mustaly-Kalimi","sequence":"first","affiliation":[{"name":"Rosalind Franklin University of Medicine and Science"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyssa M.","family":"Littlefield","sequence":"additional","affiliation":[{"name":"Rosalind Franklin University of Medicine and Science"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grace E.","family":"Stutzmann","sequence":"additional","affiliation":[{"name":"Rosalind Franklin University of Medicine and Science"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2018,9,14]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.23-12-05088.2003"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2016.12.034"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2008.09.004"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2017.09.056"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2011.08.013"},{"key":"e_1_3_2_7_2","first-page":"178.e17","article-title":"Calcium hypothesis of Alzheimer's disease and brain aging: a framework for integrating new evidence into a comprehensive theory of pathogenesis","volume":"13","author":"Arancio O","year":"2017","unstructured":"Arancio O, , Bezprozvanny I, , Berger T, , Bouteiller JM, , Carrillo M, , Disterhoft J, , Foskett K, , Khachaturian AS, , LaFerla F, , Landfield PW, , Masliah E, , Mattson M, , Michaelis ML, , Nixon R, , Snyder H, , Stutzmann GE, , Thibault O, , Yang A, , Khachaturian ZS, , and Scholz K. 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