<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Perez GI</submitter><funding>NIA NIH HHS</funding><pagination>5229-34</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1817832</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>104(12)</volume><pubmed_abstract>The menopausal transition in human females, which is driven by a loss of cyclic ovarian function, occurs around age 50 and is thought to underlie the emergence of an array of health problems in aging women. Although mice do not undergo a true menopause, female mice exhibit ovarian failure long before death because of chronological age and subsequently develop many of the same age-associated health complications observed in postmenopausal women. Here we show in mice that inactivation of the proapoptotic Bax gene, which sustains ovarian lifespan into advanced age, extends fertile potential and minimizes many age-related health problems, including bone and muscle loss, excess fat deposition, alopecia, cataracts, deafness, increased anxiety, and selective attention deficit. Further, ovariectom</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Absence of the proapoptotic Bax protein extends fertility and alleviates age-related health complications in female mice.</pubmed_title><pmcid>PMC1817832</pmcid><funding_grant_id>R01/R37-AG012279</funding_grant_id><funding_grant_id>R37 AG012279</funding_grant_id><funding_grant_id>R01 AG012279</funding_grant_id><pubmed_authors>Grynpas M</pubmed_authors><pubmed_authors>Hunt P</pubmed_authors><pubmed_authors>Perez GI</pubmed_authors><pubmed_authors>Wise L</pubmed_authors><pubmed_authors>Bechard A</pubmed_authors><pubmed_authors>Roder J</pubmed_authors><pubmed_authors>Kanisek M</pubmed_authors><pubmed_authors>Tilly JL</pubmed_authors><pubmed_authors>Lipina T</pubmed_authors><pubmed_authors>Jurisicova A</pubmed_authors><pubmed_authors>Takai Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Absence of the proapoptotic Bax protein extends fertility and alleviates age-related health complications in female mice.</name><description>The menopausal transition in human females, which is driven by a loss of cyclic ovarian function, occurs around age 50 and is thought to underlie the emergence of an array of health problems in aging women. Although mice do not undergo a true menopause, female mice exhibit ovarian failure long before death because of chronological age and subsequently develop many of the same age-associated health complications observed in postmenopausal women. Here we show in mice that inactivation of the proapoptotic Bax gene, which sustains ovarian lifespan into advanced age, extends fertile potential and minimizes many age-related health problems, including bone and muscle loss, excess fat deposition, alopecia, cataracts, deafness, increased anxiety, and selective attention deficit. Further, ovariectom</description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Mar</publication><modification>2025-04-05T10:04:51.33Z</modification><creation>2019-03-27T02:03:32Z</creation></dates><accession>S-EPMC1817832</accession><cross_references><pubmed>17360389</pubmed><doi>10.1073/pnas.0608557104</doi></cross_references></HashMap>