The following research study abstracts shown the promising potential of Colostrinin.
These abstract are for information sharing purposes only and do not intend to suggest
or imply that products containing Colostrunin can prevent, treat or cure any diseases.
Reported in the Journal of Alzheimer's Disease
J Alzheimers Dis. 2004 Feb;6(1):17-26.
Colostrinin (a naturally occurring, proline-rich polypeptide mixture) in the treatment
of Alzheimer's disease.
Bilikiewicz A, Gaus W.
Source
Clinic for Psychiatric Diseases, Medical University of Gdansk, Gdansk.
Abstract
This study was designed to confirm or negate findings from earlier trials demonstrating
that Colostrinin, a novel compound derived from ewes' colostrum, has potential in
the treatment of mild or moderate Alzheimer's Disease (AD). 105 patients were recruited
from six psychiatric centres in Poland. The trial consisted of a 15 week double-blind
phase comparing Colostrinin with placebo, followed by a second 15 week open labelled
phase when all patients received Colostrinin. The dosage of Colostrinin was 100 microg
on alternate days for three weeks followed by two weeks drug-free. This cycle was
repeated three times for each phase. The primary outcome measures used were Alzheimer's
Disease Assessment Scale-cognitive portion (ADAS-cog) and Clinical Global Impression
of Change (CGIC). Secondary outcome measures were Instrumental Activities of Daily
Living (IADL); Mini-Mental State Examination (MMSE); ADAS-non cognitive test (ADAS-non
cog); and overall Patient Response. The main outcome measures were assessed at week
15 when active was compared with placebo but all parameters were evaluated at baseline,
week 15 and week 30. Two separate statistical analyses were undertaken, a Full Sample
Analysis (FSA) in which all missing values were replaced with the worst result observed
and a Valid for Efficacy (VFE) analysis in which those patients who had serious protocol
violations were excluded. This resulted in 14 patients being excluded from the VFE-analysis.
The FSA analysis at week 15 showed a stabilizing effect of Colostrinin on cognitive
function in ADAS-cog (p = 0.02) and on daily function in IADL (p = 0.02). The overall
patient response was also in favour of the active (p = 0.03). Patients graded as
mild on entry also showed a superior response of ADAS-cog compared with more advanced
cases (p = 0.01). Evidence from this study indicates an early beneficial effect on
cognitive symptoms and daily function. Colostrinin has potential value in the treatment
AD.
PMID: 15004324 [PubMed - indexed for MEDLINE] US National Library of Medicine,
National Institutes of Health.
Copyright 2008 www.881sg.com. All rights reserved
Reported in Journal of Nutrition, Health and Aging. 2009 Jun;13(6):522-7.
J Nutr Health Aging. 2009 Jun;13(6):522-7.
The protective effects of the nutraceutical, colostrinin, against Alzheimer's disease,
is mediated via prevention of apoptosis in human neurones induced by aggregated beta-amyloid.
Douraghi-Zadeh D, Matharu B, Razvi A, Austen B.
Source
Neurodegeneration Unit, Basic Medical Sciences, St. George's, University of London,
Cranmer Terrace, Tooting, London, UK.
Abstract
OBJECTIVE:
It has previously been demonstrated that oral administration of ovine Colostrinin
(CLN), a proline-rich polypeptide isolated from ovine colostrum, can effectively
treat Alzheimer's disease patients. This study aims to determine whether CLN has
effects on the aggregation and toxicity of synthetic beta-amyloid (Abeta), implicated
as a causative agent of AD.
DESIGN AND MEASUREMENTS:
Using cell assays, we examined if pre-treatment of neuronal cells with CLN confers
protection.
RESULTS:
The data from cytotoxicity assays (using MTT and LDH) demonstrated that pre-treatment
of human neuronal SHSY-5Y cells with 5 microg/ml CLN, for 24 hours, confers neuroprotection
against Abeta-induced neurotoxicity. Twenty-four hour pre-treatment with 5 microg/ml
CLN was also shown to reduce Abeta 1-40-induced apoptosis in human neuronal cells
as determined via qualitative and quantitative apoptosis assays.
CONCLUSION:
The neuroprotection conferred with CLN pre-treatment was reduced with the Fas ligand
(FasL) binding antibody Nok1, suggesting that the effects of CLN may involve a Fas:soluble
FasL interaction. These findings indicate that CLN could possibly play a role in
the prevention of AD pathogenesis, though the inhibition of Fas-mediated apoptosis.
Comment in
J Nutr Health Aging. 2010;14(4):336.
PMID: 19536420 [PubMed - indexed for MEDLINE] US National Library of Medicine,
National Institutes of Health.
Reported in Journal of Nutrition, Health and Aging. 2009 Mar;13(3):235-41.
J Nutr Health Aging. 2009 Mar;13(3):235-41.
New insights into clinical trial for Colostrinin in Alzheimer's disease.
Szaniszlo P, German P, Hajas G, Saenz DN, Kruzel M, Boldogh I.
Source
Department of Microbiology and Immunology, University of Texas Medical Branch at
Galveston, Galveston, Texas 77555, USA.
Abstract
BACKGROUND:
The pathomechanism of Alzheimer's disease (AD) is multifactorial although the most
popular hypotheses are centered on the effects of the misfolded, aggregated protein,
amyloid beta (Abeta) and on Tau hyperphosphorylation.
OBJECTIVES:
Double blinded clinical trials were planned to demonstrate the effect of Colostrinin
(CLN) on instrumental daily activities of AD patients. The potential molecular mechanisms
by which CLN mediates its effects were investigated by gene expression profiling.
METHODS:
RNAs isolated from CLN-treated cells were analyzed by high-density oligonucleotide
arrays. Network and pathway analyses were performed using the Ingenuity Pathway Analysis
software.
RESULTS:
The Full Sample Analysis at week 15 showed a stabilizing effect of CLN on cognitive
function in ADAS-cog (p = 0.02) and on daily function in IADL (p = 0.02). The overall
patient response was also in favor of CLN (p = 0.03). Patients graded as mild on
entry also showed a superior response of ADAS-cog compared to more advanced cases
(p = 0.01). Data derived from microarray network analysis show that CLN elicits highly
complex and multiphasic changes in the cells' transcriptome. Importantly, transcriptomal
analysis showed that CLN alters gene expression of molecular networks implicated
in Abeta precursor protein synthesis, Tau phosphorylation and increased levels of
enzymes that proteolitically eliminate Abeta. In addition, CLN enhanced the defense
against oxidative stress and decreased expression of inflammatory chemokines and
cytokines, thereby attenuating inflammatory processes that precede Alzheimer's and
other neurological diseases.
CONCLUSION:
Together these data suggest that CLN has promising potential for clinical use in
prevention and therapy of Alzheimer's and other age-associated central nervous system
diseases.
PMID: 19262960 [PubMed - indexed for MEDLINE] US National Library of Medicine,
National Institutes of Health.
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