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Feedback on a feedback loop: the hypothalamic-pituitary-gonadal axis.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Atwood, Craig S. Smith, Mark A. Bowen, Richard L. |
| Copyright Year | 2005 |
| Abstract | Recent evidence indicates that transthyretin (TTR), the major transport protein for thyroxine [1] and retinol binding protein [2], plays important roles in amyloidβ (Aβ) metabolism. Transthyretin has been demonstrated to bind Aβ in vitro [3,4] andin vivo [5,6], colocalize in Aβ plaques and within neurons containing intracellular Aβ [7], and recent evidence suggests it might act as a transport protein for A β. Additionally, sAβPP-driven expression of transthyretin appears to be necessary for protection against A β induced neuronal death [7]. Therefore, the regulation of the expression of TTR may have important consequences for the deposition of Aβ in the brain. The findings of Tang and colleagues reported in JAD [8] that 17β-estradiol increases the gene expression of TTR in ovariectomized mice implicates reproductive hormones in the regulation of amyloid transport and deposition. While the sex steroids are undoubtedly important for brain function, they are controlled by a complex feedback loop that is made up of numerous other hormones including: gonadotropin releasing hormone (GnRH); the gonadotropinsluteinizing hormone |
| Starting Page | 1 |
| Ending Page | 2 |
| Page Count | 2 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://content.iospress.com/download/journal-of-alzheimers-disease/jad00405?id=journal-of-alzheimers-disease/jad00405 |
| PubMed reference number | 15750209v1 |
| Volume Number | 7 |
| Issue Number | 1 |
| Journal | Journal of Alzheimer's disease : JAD |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Axis vertebra Carrier Proteins Cessation of life Gene Expression Gonadal structure Gonadorelin Gonadotropins In Vitro [Publication Type] Prealbumin Reproduction Senile Plaques Steroids Vitamin A levothyroxine |
| Content Type | Text |
| Resource Type | Article |
