Increased O-GlcNAcylation reduces pathological tau without affecting its normal phosphorylation in a mouse model of tauopathy.

Neurofibrillary tangles (NFT), mainly consisting of fibrillar aggregates of hyperphosphorylated tau, are a defining pathological feature of Alzheimer's Disease and other tauopathies. Progressive accumulation of tau into NFT is considered to be a toxic cellular event causing neurodegeneration. Tau is subject to O-linked N-acetylglucosamine (O-GlcNAc) modification and O-GlcNAcylation of tau has been suggested to regulate tau phosphorylation.

Distribution of estrogen receptor alpha and beta in the mouse central nervous system: in vivo autoradiographic and immunocytochemical analyses.

Although the distribution of estrogen receptor beta (ERbeta) immunoreactivity in the rat central nervous has been reported, no such data are available in the mouse. The present study used in vivo autoradiography utilizing a (125)I-estrogen that has equal binding affinity for both receptors as well as immunohistochemistry for ERbeta and ERalpha, to investigate and compare the distribution of the two ERs in the mouse CNS. The use specific antisera against ERalpha and ERbeta allowed us to evaluate the contribution of these receptors to the binding detected with autoradiography.

Neuroprotection by estrogen in animal models of global and focal ischemia.

Estrogen has been demonstrated to protect against brain injury, neurodegeneration, and cognitive decline. Furthermore, estrogen seems to specifically protect cortical and hippocampal neurons from ischemic injury. Here our data evaluating the neuroprotective effects of estrogens, the selective estrogen receptor modulators (SERMs), and estrogen receptor alpha- and beta-selective ligands in animal models of ischemic injury are discussed.

Estrogen regulation of neurokinin B gene expression in the mouse arcuate nucleus is mediated by estrogen receptor alpha.

Neurokinin B (NKB) gene expression is elevated in the infundibular (arcuate) nucleus of the hypothalamus in postmenopausal women. Estrogen replacement decreases both the number of NKB mRNA-expressing neurons and the level of expression within individual cells. Similarly, NKB gene expression is elevated in ovariectomized rats and reduced after estrogen treatment.

Anosmin-1 immunoreactivity during embryogenesis in a primitive eutherian mammal.

Kallmann syndrome is hypogonadotropic hypogonadism coupled with anosmia. A morphological study found that the endocrine disorder in X-linked Kallmann syndrome is due to failed migration of gonadotropin releasing-hormone (GnRH) neurons from the olfactory placode to the brain during development. Anosmia results from agenesis of the olfactory bulbs and tracts.

Estrogen modulates oxytocin gene expression in regions of the rat supraoptic and paraventricular nuclei that contain estrogen receptor-beta.

Oxytocin is an important modulator of female reproductive functions including parturition, lactation and maternal behavior, while vasopressin regulates water balance and acts as a neurotransmitter. For decades, it has been suggested that estrogen regulates the production and/or release of oxytocin and vasopressin in the rodent brain. Although several studies demonstrated that estrogen can modulate vasopressin mRNA levels in regions known to contain estrogen receptor (ER), such as the bed nucleus of the stria terminalis and medial amygdala, data from the paraventricular and supraoptic nuclei were inconclusive.

Estrogen-binding sites and their functional capacity in estrogen receptor double knockout mouse brain.

Early studies found estrogen-binding sites in the ER knockout (ERalphaKO) mouse brain, suggesting a splice variant of ERalpha or another ER. The discovery of ERbeta suggested that binding was due to ERbeta, although questions about an ERgamma remained. To test this hypothesis, ERbetaKO mice were generated and crossed with ERalphaKO mice, and ERalpha/betaKO animals were used for in vivo binding studies with [(125)I]estrogen.