Duncan Crow
Wholistic Consultant
http://members.shaw.ca/SomaLife-gHP/HGH_neuro_medline.html
HGH deficiency in neurodegenerative disorders
In each of
these cases you can go to the Medline site
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
and enter the PMID number to bring up the abstract.
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IGF-1 May Stimulate Brain Function
If grandpa's been "slipping" a bit in his twilight years, it may be that he's lacking the hormones he needs to keep his brain functioning efficiently.
Researchers in the Netherlands measured insulin-like growth factor 1 (IGF-1) levels in a group of healthy older men aged 69-76, and evaluated their performance on a battery of tests designed to measure cognitive ability. IGF-1 mediates the stimulatory effect of growth hormone (GH) on tissues, and also triggers its own anabolic effects. Age-related decline of IGF-1 is associated with the breakdown of muscle and bone mass, increased body fat, and other types of physiological degeneration.
The investigators in this study found a positive correlation between IGF-1 levels and perceptual motor and mental processing speed - a relationship independent of both education level and age. The implications are important because they signify a possible relationship between hormone levels and "the rate at which cognitive operations can be executed in the brain."
"This finding suggests that the GH/IGF-1 axis may play a role in the age-related decline of certain cognitive functions," researchers concluded. Results bolster previous studies linking growth-hormone deficiency with cognitive and memory impairment in both children and adults.
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J Neuropathol Exp Neurol 2000 Jul;59(7):575-84
PMID: 10901228 [PubMed - indexed for MEDLINE]
Insulin-like growth factor-I promotes myelination of peripheral sensory axons.
Russell JW, Cheng HL, Golovoy D.
Department of Neurology, Veterans Administration Medical Center, University of Michigan, Ann Arbor 48109, USA.
BACKGROUND: Insulin-like growth factor-I (IGF-I) in vivo or in the presence of other permissive factors can promote myelination in the central nervous system.
CONCLUSIONS: IGF-I is important in myelination and is critical not only for initial SC ensheathment of the axon and upregulation of myelin proteins, but also for sustained myelination. Furthermore, IGF-I associated axonal size is not the sole determinant for myelination.
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Ann N Y Acad Sci 1999 Sep 14;883:124-30
PMID: 10586238 [PubMed - indexed for MEDLINE]
IGF-I promotes peripheral nervous system myelination.
Cheng HL, Russell JW, Feldman EL.
Department of Neurology, University of Michigan, Ann Arbor 48109-0588, USA.
Insulin-like growth factor-I (IGF-I) promotes the proliferation and differentiation of Schwann cells (SC). Continued IGF-I exposure leads to enhanced P0 expression and long-term myelination. No myelination occurs in the absence of IGF-I. These data imply that IGF-I is critical not only for SC attachment and ensheathment of axons but also for long-term myelination.
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Neuroreport 1997 Sep 8;8(13):2871-6
PMID: 9376522 [PubMed - indexed for MEDLINE]
The insulin-like growth factors I and II stimulate proliferation of different types of Schwann cells.
Sondell M, Fex-Svenningsen A, Kanje M.
Department of Animal Physiology, Lund University, Sweden.
IGF-II enhanced proliferation of Schwann cells surrounding unmyelinated nerve fibres. In contrast, truncated IGF-I promoted proliferation of Schwann cells of myelinated nerve fibres while insulin increased proliferation of both cell types.
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J Neurobiol 1999 Dec;41(4):540-8 Related Articles, Links
PMID: 10590177 [PubMed - indexed for MEDLINE]
Insulin-like growth factor-I prevents caspase-mediated apoptosis in Schwann cells.
Delaney CL, Cheng HL, Feldman EL.
Department of Neurology, University of Michigan, 200 Zina Pitcher Place, 4414 Kresge III, Ann Arbor, Michigan 48109, USA.
BACKGROUND: Both neurons and glia succumb to programmed cell death (PCD) when deprived of growth factors at critical periods in development or following injury. Insulin-like growth factor-I (IGF-I) prevents apoptosis in neurons in vitro.
CONCLUSIONS: These results suggest that IGF-I rescues Schwann Cells from apoptosis via PI 3-K signaling which is upstream from caspase activation. Copyright 1999 John Wiley & Sons, Inc.
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Neurology 1997 Dec;49(6):1621-30
PMID: 9409357 [PubMed - indexed for MEDLINE]
Effect of recombinant human insulin-like growth factor-I on progression of ALS. A placebo-controlled study. The North America ALS/IGF-I Study Group.
Lai EC, Felice KJ, Festoff BW, Gawel MJ, Gelinas DF, Kratz R, Murphy MF, Natter HM, Norris FH, Rudnicki SA.
Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.
Recombinant human insulin-like growth factor-I slowed the progression of functional impairment and the decline in health-related quality of life in patients with ALS with no medically important adverse effects.
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Pharmacoeconomics 1999 Feb;15(2):179-95
Cost effectiveness of recombinant human insulin-like growth factor I therapy in patients with ALS.
Ackerman SJ, Sullivan EM, Beusterien KM, Natter HM, Gelinas DF, Patrick DL.
Covance Health Economics and Outcomes Services Inc., Washington, DC, USA. stacey.ackerman@covance.com
OBJECTIVE: Amyotrophic lateral sclerosis (ALS) is a fatal, degenerative neuromuscular disease characterised by a progressive loss of voluntary motor activity. Recombinant human insulin-like growth factor I (rhIGF-I) has been shown to be useful in treating ALS.
CONCLUSIONS: Treatment with rhIGF-I is most cost effective in ALS patients who are either in earlier stages of the disease or progressing rapidly. The cost effectiveness of rhIGF-I therapy compares favourably with treatments for other chronic progressive diseases.
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