{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T16:33:56Z","timestamp":1777394036505,"version":"3.51.4"},"reference-count":0,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2011,12,12]],"date-time":"2011-12-12T00:00:00Z","timestamp":1323648000000},"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":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2011,12,12]]},"abstract":"<jats:p>\n                    We have contended that senile conditions\u2014illnesses after age 60 and fully age-penetrating, such as tooth, hearing or memory loss\u2014are not distinct \u201cdiseases\u201d in medical nature, because they are caused by aging. Since the pace of aging varies among individuals and is much influenced by risk factors, senile conditions will only affect some but not all elderly. However, perhaps due to its unusually heavy burdens and tremendous social pressures, senile dementia (SD) has been singled out from other senile conditions and redefined as a curable \u201cdisease\u201d (Alzheimer's). This highly popular definition has thus opened a Pandora's box that has been confusing us up until now and warrants further scrutiny. In this article we discuss: a) what should we logically look for in SD beyond \u201cpathogenic\u201d factors?; b) why Ca\n                    <jats:sup>2+<\/jats:sup>\n                    , a central regulator in neurotransmission, should be the primary player in SD; c) why the functionality of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling, or its vibrant wave frequency and amplitude, must undergo down-regulation during aging, though this is intriguingly accompanied by an increase of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u201clevels\u201d; d) why intervention for SD should target Ca\n                    <jats:sup>2+<\/jats:sup>\n                    function by promoting energy metabolisms and by Ca\n                    <jats:sup>2+<\/jats:sup>\n                    agonists such as caffeine and nicotine, but not by \u201cantagonists\u201d as widely believed; and e) why our study should focus on aging, not \u201ccell death\u201d, a seemingly attractive paradigm but perhaps too late for intervention. We also seek answers for why unproven hypotheses can become dogmas and inhibit self-correcting mechanisms of science.\n                  <\/jats:p>","DOI":"10.3233\/jad-2011-111142","type":"journal-article","created":{"date-parts":[[2018,5,16]],"date-time":"2018-05-16T04:34:37Z","timestamp":1526445277000},"page":"679-689","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["What to Look for Beyond \u201cPathogenic\u201d Factors in Senile Dementia? A Functional Deficiency of Ca\n                    <sup>2+<\/sup>\n                    Signaling"],"prefix":"10.1177","volume":"27","author":[{"given":"Ming","family":"Chen","sequence":"first","affiliation":[{"name":"Aging Research Laboratory, Bay Pines VA Healthcare System, Bay Pines, Florida, USA"},{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, FL, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huey T.","family":"Nguyen","sequence":"additional","affiliation":[{"name":"Aging Research Laboratory, Bay Pines VA Healthcare System, Bay Pines, Florida, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darrell R.","family":"Sawmiller","sequence":"additional","affiliation":[{"name":"Aging Research Laboratory, Bay Pines VA Healthcare System, Bay Pines, Florida, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2011,12,12]]},"container-title":["Journal of Alzheimer\u2019s Disease"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/JAD-2011-111142","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/JAD-2011-111142","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T10:02:16Z","timestamp":1777370536000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.3233\/JAD-2011-111142"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2011,12,12]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2011,12,12]]}},"alternative-id":["10.3233\/JAD-2011-111142"],"URL":"https:\/\/doi.org\/10.3233\/jad-2011-111142","relation":{},"ISSN":["1387-2877","1875-8908"],"issn-type":[{"value":"1387-2877","type":"print"},{"value":"1875-8908","type":"electronic"}],"subject":[],"published":{"date-parts":[[2011,12,12]]}}}