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- W2000474839 abstract "Endocrine disruption is a concept and principle whose origins can be traced to the beginnings of the environmental movement in the 1960s. It began with puzzlement about and the flaring of research on the decline of wildlife, particularly avian species. The proposed causes accented pesticides, especially persistent organochlorines such as DDT. Its scope gradually widened beyond pesticides, and, as endocrine disruption offered an explanation for the wildlife phenomena, it seemed to explain, as well, changes in fertility and disorders of male reproduction such as testicular cancer. Once disturbed gonadal hormone function became the most likely explanation, it provoked other questions. The most challenging arose because of how critical gonadal hormones are to brain function, especially as determinants of brain sexual differentiation. Pursuit of such connections has generated a robust literature embracing a broad swath of chemical classes. How endocrine disrupting chemicals influence the adult and aging brain is a question, so far mostly ignored because of the emphasis on early development, that warrants vigorous investigation. Gonadal hormones are crucial to optimal brain function during maturity and even senescence. They are pivotal to the processes of neurogenesis. They exert protective actions against neurodegenerative disorders such as dementia and support smoothly functioning cognitive activities. The limited research conducted so far on endocrine disruptors, aging, and neurogenesis argues that they should be overlooked no longer." @default.
- W2000474839 created "2016-06-24" @default.
- W2000474839 creator A5086241075 @default.
- W2000474839 date "2011-06-01" @default.
- W2000474839 modified "2023-10-01" @default.
- W2000474839 title "Endocrine disruptors as a threat to neurological function" @default.
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- W2000474839 doi "https://doi.org/10.1016/j.jns.2011.03.014" @default.
- W2000474839 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3090512" @default.
- W2000474839 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21474148" @default.
- W2000474839 hasPublicationYear "2011" @default.
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