> I will like to know about Alzheimer's disease and rHGH. I am a
> Surgeon working in Tampico Mexico and have a lot of interest in this
> Thank you for your attention
> DR JS Ramirez Rosas
> [Hello Dr. Ramirez Rosas... There is not much that I really know about
> how recombinant human growth hormone (rHGH) affects Alzheimer's. In
> general, growth hormone helps to preserve the nervous system, so it
> might help to halt or retard the advance of Alzheimer's, to the extent
> that Alzheimer's is a loss of neurons.
Specific information from Medline on how HGH elevation regenerates
myelin is found here, in the neurodegeneratives section:
[I copy the neurodegeneratives section below...Thanks. - Ellis]
In each of these cases you can go to the Medline site
and enter the PMID number to bring up the abstract.
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.
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
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.
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.
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
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
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
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.
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.
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.
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.