Post by Max on Jun 12, 2005 18:56:43 GMT -5
Vitamin A and the brain
Vitamin D and the brain
(Ro)accutane induced insulin resistance/ decreased entry through the blood brain barrier, and the brain
Brain insulin resistance is suggested to contribute to cognitive impairment [6]. Reduced levels of insulin produced in brain can lead to death of key brain cells, and may contribute to pathologies like Alzheimers disease [3]. Insulin deficiency within the brain in insulin knockout mice (I(-/-)). The I(-/-) exhibited hyperphosphorylation of tau, at threonine 231, and neurofilament. In addition, we showed hyperphosphorylation of c-Jun N-terminal kinase (JNK) and glycogen synthase kinase 3 beta (GSK-3 beta) at serine 9. Extracellular signal-regulated kinase 1 (ERK 1) showed decrease in phosphorylation, whereas ERK 2 showed no changes. Ultrastructural examination demonstrated swollen mitochondria, endoplasmic reticulum, and Golgi apparatus, and dispersion of the nuclear chromatin. Microtubules showed decrease in the number of intermicrotubule bridges and neurofilament presented as bunches. Thus, lack of insulin brain stimulation induces JNK hyperphosphorylation followed by hyperphosphorylation of tau and neurofilament, and ultrastructural cellular damage, that over time may induce decrease in cognition and learning disabilities [4].
Growth hormone and the brain
A GH/IGF-1 deficiency is suggested due to vitamin A induced significant interaction with the GH axis. The IGF-1 receptors are expressed in cells in the brain.
Thyroid hormone and the brain
Progesterone and the brain
Dihydrotestosterone and the brain: expression and binding in pituitary, hypothalamus, amygdala and cortex
The enzyme 5alpha-reductase (5alpha-R) is present in many mammalian tissues, including the brain. The physiological importance of 5alpha-R in the brain derives from its capability to convert testosterone (T) to a more potent androgen, dihydrotestosterone (DHT), and to convert progesterone to its 5alpha-reduced derivative, precursors of allopregnanolone, potent allosteric modulator of the gamma-aminobutyric acid receptor (GABA(A)-R). 5alpha-R occurs as two isoforms, 5alpha-R type 1 (5alpha-R1) and 5alpha-R type 2 (5alpha-R2) [1].
Dihydrotestosterone (DHT) binding was measured in cytosols from brain regions and pituitary of adult female rats and, with the addition of ventral prostate, in adult male rats. Two types of binding were distinguished: one, saturable at concentration of DHT greater than or equal to 5 X 10(-9) M and an unsaturable component. In intact males saturable (limited capacity) binding was detected only in ventral prostate cytosol; 3 days after orchidectomy the saturable binding sites increase 3-fold in prostate and in pituitary, hypothalamus, amygdala and cortex to detectable levels in approximately the same abundance as in females. There were significant differences in the affinities of the limited capacity binding reactions in cytosols of different tissues though all were in the order of magnitude, 10(-9) M DHT. The affinity in pituitary cytosol was lower than in brain regions with the single exception of female amygdala in which the affinity was significantly lower than in cytosol of the same region from 3-day castrate males. The specificity of the limited capacity binding was investigated by competition between [3h]DHT and unlabelled steroids; the most effective competitors were potent androgen agonists and antagonists [2].
Vitamin D and the brain
(Ro)accutane induced insulin resistance/ decreased entry through the blood brain barrier, and the brain
Brain insulin resistance is suggested to contribute to cognitive impairment [6]. Reduced levels of insulin produced in brain can lead to death of key brain cells, and may contribute to pathologies like Alzheimers disease [3]. Insulin deficiency within the brain in insulin knockout mice (I(-/-)). The I(-/-) exhibited hyperphosphorylation of tau, at threonine 231, and neurofilament. In addition, we showed hyperphosphorylation of c-Jun N-terminal kinase (JNK) and glycogen synthase kinase 3 beta (GSK-3 beta) at serine 9. Extracellular signal-regulated kinase 1 (ERK 1) showed decrease in phosphorylation, whereas ERK 2 showed no changes. Ultrastructural examination demonstrated swollen mitochondria, endoplasmic reticulum, and Golgi apparatus, and dispersion of the nuclear chromatin. Microtubules showed decrease in the number of intermicrotubule bridges and neurofilament presented as bunches. Thus, lack of insulin brain stimulation induces JNK hyperphosphorylation followed by hyperphosphorylation of tau and neurofilament, and ultrastructural cellular damage, that over time may induce decrease in cognition and learning disabilities [4].
Growth hormone and the brain
A GH/IGF-1 deficiency is suggested due to vitamin A induced significant interaction with the GH axis. The IGF-1 receptors are expressed in cells in the brain.
Thyroid hormone and the brain
Progesterone and the brain
Dihydrotestosterone and the brain: expression and binding in pituitary, hypothalamus, amygdala and cortex
The enzyme 5alpha-reductase (5alpha-R) is present in many mammalian tissues, including the brain. The physiological importance of 5alpha-R in the brain derives from its capability to convert testosterone (T) to a more potent androgen, dihydrotestosterone (DHT), and to convert progesterone to its 5alpha-reduced derivative, precursors of allopregnanolone, potent allosteric modulator of the gamma-aminobutyric acid receptor (GABA(A)-R). 5alpha-R occurs as two isoforms, 5alpha-R type 1 (5alpha-R1) and 5alpha-R type 2 (5alpha-R2) [1].
Dihydrotestosterone (DHT) binding was measured in cytosols from brain regions and pituitary of adult female rats and, with the addition of ventral prostate, in adult male rats. Two types of binding were distinguished: one, saturable at concentration of DHT greater than or equal to 5 X 10(-9) M and an unsaturable component. In intact males saturable (limited capacity) binding was detected only in ventral prostate cytosol; 3 days after orchidectomy the saturable binding sites increase 3-fold in prostate and in pituitary, hypothalamus, amygdala and cortex to detectable levels in approximately the same abundance as in females. There were significant differences in the affinities of the limited capacity binding reactions in cytosols of different tissues though all were in the order of magnitude, 10(-9) M DHT. The affinity in pituitary cytosol was lower than in brain regions with the single exception of female amygdala in which the affinity was significantly lower than in cytosol of the same region from 3-day castrate males. The specificity of the limited capacity binding was investigated by competition between [3h]DHT and unlabelled steroids; the most effective competitors were potent androgen agonists and antagonists [2].
