Regular ArticleRole of Sex Steroids on the Survival, Neuritic Outgrowth of Neurons, and Dopamine Neurons in Cultured Preoptic Area and Hypothalamus
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Association between CYP17A1 rs3824755 and rs743572 gene polymorphisms and Alzheimer's disease in the Chinese Han population
2016, Neuroscience LettersCitation Excerpt :Age-related decline in testosterone levels has also been associated with increased AD risk in men [12]. Testosterone exerts neuroprotective effects by inhibiting Aβ accumulation; promoting neuronal growth, synaptic function, and axonal regeneration; and protecting against neuronal loss [19,30]. Various genes involved in the biosynthesis and metabolism of sex steroids have been linked to AD; one of these, CYP17A1, is responsible for testosterone and estrogen production.
Gender, sex steroid hormones, and Alzheimer's disease
2013, Hormones and BehaviorCitation Excerpt :Such beneficial neural actions of androgens include: (1) promotion of neuron growth, axonal regeneration, and synaptic function, (2) protection against neuron cell loss, and (3) regulation of AD-related pathology including Aβ accumulation. In the first case, androgens have a variety of growth-promoting and maturational effects on neurons in a range of paradigms (Arai, 1991; Brannvall et al., 2005; Cooke et al., 1998; Gorski, 1985; Kawashima and Takagi, 1994; Lustig, 1994; Matsumoto, 1991). In addition, androgens are potent facilitators of spine density and synaptic function, including regulation of long-term potentiation in the hippocampus (Garcia-Segura et al., 1994; Hajszan et al., 2008; Hatanaka et al., 2009; MacLusky et al., 2004; Matsumoto, 2001; Matsumoto et al., 1988; Pouliot et al., 1996; Schulz and Korz, 2010).
Epigenetic changes brought about by perinatal stressors: A brief review of the literature
2012, Journal of Pharmacological and Toxicological MethodsCitation Excerpt :Dörner et al. (1991) have suggested that prenatal stress may operate in male-typical sexual behavior in a similar manner in humans. Sexual dimorphisms have been identified in the size of the preoptic nucleus, stria terminalis, amygdala, hippocampus (Kawashima & Takagi, 1994), anterior commissure (Jones et al., 1997) and certain nuclei of the ventromedial nucleus of the hypothalamus (VMH) (Flanagan-Cato, 2000), all of which suggests numerous structural sexual dimorphisms. Certain other cell types in the brain exhibit dimorphic properties as well.
Neuroprotective actions of brain aromatase
2009, Frontiers in NeuroendocrinologyCitation Excerpt :While there is some evidence for a degenerative role of androgens in development and sexual differentiation [9], there appear to be many more reports confirming the neuroprotective properties of androgens in vitro and in adult model systems. Several in vitro studies demonstrate that dehydroepiandrosterone (DHEA) enhances neuronal and glial survival [201,32], while testosterone (T) increases neuronal survival, the number and receptive field of neurite processes, and neurotransmitter output [130,248]. Also, T has been shown to increase neurite length [199], angiogenesis [133], and neurogenesis [133,7,143].
Cellular mechanisms of estradiol-mediated masculinization of the brain
2008, Journal of Steroid Biochemistry and Molecular BiologyInsulin-like growth factor-I receptor and estrogen receptor crosstalk mediates hormone-induced neurite outgrowth in PC12 cells
2004, Brain ResearchCitation Excerpt :Seven-day treatments with IGF-I in PC12-ER and PC12-C cells, and with E2 in PC12-ER cells, increased the percentage of process-bearing cells and the absolute neurite length per cell. PC12 cells transfected with the pCMV-neo vector, without the ERα gene, also elaborated neurites in response to IGF-I. Although studies in dissociated cells and in vivo have demonstrated that IGF-I [1,35,36] or E2 alone [1,20,27,28,30] can stimulate process outgrowth, our new data demonstrate that crosstalk between ER and IGF-IR is necessary for E2- and IGF-I-stimulated neurite outgrowth within this homogenous cell system. Specifically, inhibition of ER with the antagonist ICI blocks the neurite promoting effects of both E2 and IGF-I. Likewise, inhibition of IGF-IR with the antagonist JB1 blocks the neurite promoting effects of both IGF-I and E2.