Medical bioremediation of age-related diseases. - novoseek
"Catabolic insufficiency in humans leads to the gradual accumulation of a number of pathogenic compounds associated with age-related diseases, including atherosclerosis, Alzheimer's disease, and macular degeneration. Removal of these compounds is a widely researched therapeutic option, but the use of antibodies and endogenous human enzymes has failed to produce effective treatments, and may pose risks to cellular homeostasis. Another alternative is 'medical bioremediation,' the use of microbial enzymes to augment missing catabolic functions. The microbial genetic diversity in most natural environments provides a resource that can be mined for enzymes capable of degrading just about any energy-rich organic compound. This review discusses targets for biodegradation, the identification of candidate microbial enzymes, and enzyme-delivery methods.
Effect of immunisation with Chlamydia pneumoniae recombinant major outer membrane protein on atherosclerosis development -- El Kadri et al. 96 (17): e27 -- Heart
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How Cranberry Juice Fights Bacteria That Cause Urinary Tract Infections:
Image via WikipediaHow Cranberry Juice Fights Bacteria That Cause Urinary Tract Infections:
65ZVZ9PBSDBD
Change in the expression of myelination/oligodendrocyte-related genes during puberty in the rat brain.
Image via WikipediaMap of schizophrenia distribution
Insulin resistance is associated with the pathology of Alzheimer disease. The Hisayama Study.
Insulin resistance is associated with the pathology of Alzheimer disease.
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- Mixed pathologies in brains of elderly account for memory loss and confusion (news-medical.net)
An N-terminally truncated envelope protein encoded by a human endogenous retrovirus W locus on chromosome Xq22.3.
Detection of an antigen by 6A2B2 in placenta and multiple sclerosis lesions opens the possibility that N-Trenv could be expressed in vivo
The human genome is composed of Viral DNA II: Individual proteins contain multiple viral inserts
Individual proteins, and individual translated exons within these proteins, are composed of multiple internested viral protein fragments. This is illustrated for the translated exons of DISC1 , where the different viral contributions are colour coded for each virus or phage.
Follow this link for the exons concerned
Follow this link for the exons concerned
Clusterin synergizes with IL-2 for the expansion and IFN-{gamma} production of natural killer cellsxpansion a... [J Leukoc Biol. 2010] - PubMed result
"The role of Clusterin on natural killer cells should be taken into consideration for the previously observed, diverse functions of clusterin in chronic inflammatory and autoimmune conditions". 
CSF markers of neurodegeneration in Parkinson's disease.
Significantly higher tau protein and clusterin CSF levels in the group of PD patients with disease duration of less than years probably reflect the fact that most neurodegenerative changes in PD patients occur in the initial stage of disease. 
A possible cure for Huntington's disease ?
Polyglutamine peptides, of the kind found in Huntington’s disease and other PolyQ disorders are
immunogenic, the more so with each addition of glutamine. Polyglutamine repeats are also found
in almost 2000 proteins expressed by viruses, phages, bacteria, yeasts and fungi. These include the
omnipresent Herpes virus, HSV-6 and numerous endemic or commensal bacteria, yeast or fungi.
They are also found in Lactococcal species, perhaps explaining why milk consumption has been
reported to lower the age of onset in this condition. Immune activation has indeed been observed
sixteen years prior to the onset of Huntington’s disease (see also these refs). This suggests that antibodies to these infectious agents also target the human mutant protein, causing degeneration via immune attackand inflammatory mechanism:
Immunosuppression , antibody adsorption, anti-antibody antibodies and aggressive antiviral and
antibacterial strategies might delay the onset and stem the progression of Huntington’s disease.
Download pdf
immunogenic, the more so with each addition of glutamine. Polyglutamine repeats are also found
in almost 2000 proteins expressed by viruses, phages, bacteria, yeasts and fungi. These include the
omnipresent Herpes virus, HSV-6 and numerous endemic or commensal bacteria, yeast or fungi.
They are also found in Lactococcal species, perhaps explaining why milk consumption has been
reported to lower the age of onset in this condition. Immune activation has indeed been observed
sixteen years prior to the onset of Huntington’s disease (see also these refs). This suggests that antibodies to these infectious agents also target the human mutant protein, causing degeneration via immune attackand inflammatory mechanism:
Immunosuppression , antibody adsorption, anti-antibody antibodies and aggressive antiviral and
antibacterial strategies might delay the onset and stem the progression of Huntington’s disease.
Download pdf
Alcohol Intake and Risk of Incident Psoriasis in US Women: A Prospective Study.
Non-light beer drinking linked to psoriasis
Plasma Clusterin Levels in Predicting the Occurrence of Coronary Artery Lesions in Patients With Kawasaki Disease.
Plasma Clusterin Levels in Predicting the Occurrence of Coronary Artery Lesions in Patients With Kawasaki Disease.
Beneficial effects of N-acetylcysteine in treatment resistant schizophrenia.
Beneficial effects of N-acetylcysteine in treatment resistant schizophrenia
See also
See also
Magnetic resonance spectroscopy study of the antioxidant defense system in schizophrenia.
Is it time to reassess alpha lipoic acid and niacinamide therapy in schizophrenia?
alpha lipoic acid niacinamide glutathione
DJ-1, an oncogene and causative gene for familial Parkinson's disease, is essential for SV40 transformation in mouse fibroblasts through up-regulation
Image via WikipediaDJ-1, an oncogene and causative gene for familial Parkinson's disease, is essential for Simian virus 40 transformation in mouse fibroblasts through up-regulation of c-Myc.
The human genome is composed of viral DNA
Evidence from over 2 million viral/human alignments, shows that the human genome is composed of viral DNA.
This is not just retroviruses (XMRV and HIV-1) but common viruses such as the rhinovirus, Epstein-Barr, influenza, herpes, papillomavirus, coronavirus and many more. This supports the idea, proposed over a century ago, by J.B.S.Haldane and Felix D'Herelle that viruses are responsible for the origin of life, and also the idea that viral inserts are responsible for evolutionary jumps.(the insertion of several viral genes, if passed on through the germ line, effectively creates a new being)
As if that were not interesting enough, here is the important factor , exemplified by Alzheimer's disease Bipolar disorder and schizophrenia. The insertion points of the viruses implicated as risk factors in any particular disease correspond to the locations of the genes implicated in the disease.
The more important the gene in Alzheimer's disease (and others), the more viral proteins it matches (and those of other pathogens).
These viral matches appear to cover the whole human genome, and every human protein is homologous to one virus or another.
In the human genome, these matches are characterised by millions of gapped consecutive and contiguous segments which translate into short contiguous peptide stretches (5-12 amino acids long).The older the viral insertion, the more fragmented the DNA, the shorter the protein matches,but the greater the number of human/viral homologues.
These human protein matches (vatches) are identical to those in the proteins expressed by the viruses implicated in the disease.
Because the viral protein is similar to human receptors, peptide ligands, enzymes, etc it can act as a dummy ligand or a decoy receptor, and also interfere with the interactome of its human counterpart. This is shown quite clearly in the DISC1/viral interactome
Upon infection, antibodies to the virus also risk targeting their human counterparts, which will in effect be knocked down when the antibody binds. The protein equivalent of gene knockouts. If the peptides are highly immunogenic, then cells containing the virus, or its human analogue will be targeted for destruction. This is exemplified by the fact that immunisation with tau in mice provokes the neurofibrillary tangle pathology seen in Alzheimer's disease.Tau is homologous to Herpes simplex and other viral proteins.
All of the diseases on the website pages Alzheimer's disease, Bipolar disorder, Schizophrenia, Chonic fatigue, and more, have an autoimmune component, pathogens are implicated in all, and the genes and pathogens fit together, hand in glove, for all (Bipolar disorder, Alzheimer's and schizophrenia).
Viruses (known and unsuspected culrits) are also homologous to the autoantigens in multiple sclerosis and to the mutant proteins in Huntington's disease and cystic fibrosis (see website)
This suggests that many human diseases work via this common mechanism, and therefore that most are preventable, by vaccination or elimination of the pathogen, and perhaps curable by immunosuppressant therapy.
Examples of how this works are here
A pdf of a prepublication is available at NaturePrecedings.
This is not just retroviruses (XMRV and HIV-1) but common viruses such as the rhinovirus, Epstein-Barr, influenza, herpes, papillomavirus, coronavirus and many more. This supports the idea, proposed over a century ago, by J.B.S.Haldane and Felix D'Herelle that viruses are responsible for the origin of life, and also the idea that viral inserts are responsible for evolutionary jumps.(the insertion of several viral genes, if passed on through the germ line, effectively creates a new being)
As if that were not interesting enough, here is the important factor , exemplified by Alzheimer's disease Bipolar disorder and schizophrenia. The insertion points of the viruses implicated as risk factors in any particular disease correspond to the locations of the genes implicated in the disease.
The more important the gene in Alzheimer's disease (and others), the more viral proteins it matches (and those of other pathogens).
These viral matches appear to cover the whole human genome, and every human protein is homologous to one virus or another.
In the human genome, these matches are characterised by millions of gapped consecutive and contiguous segments which translate into short contiguous peptide stretches (5-12 amino acids long).The older the viral insertion, the more fragmented the DNA, the shorter the protein matches,but the greater the number of human/viral homologues.
These human protein matches (vatches) are identical to those in the proteins expressed by the viruses implicated in the disease.
Because the viral protein is similar to human receptors, peptide ligands, enzymes, etc it can act as a dummy ligand or a decoy receptor, and also interfere with the interactome of its human counterpart. This is shown quite clearly in the DISC1/viral interactome
Upon infection, antibodies to the virus also risk targeting their human counterparts, which will in effect be knocked down when the antibody binds. The protein equivalent of gene knockouts. If the peptides are highly immunogenic, then cells containing the virus, or its human analogue will be targeted for destruction. This is exemplified by the fact that immunisation with tau in mice provokes the neurofibrillary tangle pathology seen in Alzheimer's disease.Tau is homologous to Herpes simplex and other viral proteins.
All of the diseases on the website pages Alzheimer's disease, Bipolar disorder, Schizophrenia, Chonic fatigue, and more, have an autoimmune component, pathogens are implicated in all, and the genes and pathogens fit together, hand in glove, for all (Bipolar disorder, Alzheimer's and schizophrenia).
Viruses (known and unsuspected culrits) are also homologous to the autoantigens in multiple sclerosis and to the mutant proteins in Huntington's disease and cystic fibrosis (see website)
This suggests that many human diseases work via this common mechanism, and therefore that most are preventable, by vaccination or elimination of the pathogen, and perhaps curable by immunosuppressant therapy.
Examples of how this works are here
A pdf of a prepublication is available at NaturePrecedings.
Network analysis of positional candidate genes of schizophrenia highlights…more than… myelin-related pathways
See also these papers
Network analysis of positional candidate genes of schizophrenia highlights…more than… myelin-related pathways
Network analysis of positional candidate genes of schizophrenia highlights…more than… myelin-related pathways
Structural brain alterations in schizophrenia following fetal exposure to the inflammatory cytokine interleukin-8.
Structural brain alterations in schizophrenia following fetal exposure to the inflammatory cytokine interleukin-8.
Aquaporin 4 antibody positive central nervous system autoimmunity and multiple sclerosis are characterized by a distinct profile of antibodies to herpes viruses.
Aquaporin 4 antibody positive central nervous system autoimmunity and multiple sclerosis are characterized by a distinct profile of antibodies to herpes viruses.
Streptococcal protein SIC: An anti-inflammatory virulence determinant. (Binds to Clusterin)
"SIC blocks complement-mediated hemolysis, inhibits the activity of anti-bacterial peptides and has affinity for the human plasma proteins clusterin"
Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning.
Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning.
This is a fascinating paper showing that many of the remedies in old wive's tales have a physiological and biochemical basis
This is a fascinating paper showing that many of the remedies in old wive's tales have a physiological and biochemical basis
Evaluation of an Edible Blue-Green Alga, Aphanothece sacrum, for Its Inhibitory Effect on Replication of Herpes Simplex Virus Type 2 and Influenza
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Huntingtin Is Required for Mitotic Spindle Orientation and Mammalian Neurogenesis
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Improving lupus treatment with TLR7 and TLR9 antagonists : SciBX: Science-Business eXchange
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