The Role of Spirochetes in Alzheimer's and Neurodegeneration
Alzheimer's disease has been associated with spirochetes. Quotient sensing, salt, water, temperature and antibiotic use are known triggers of biofilm formation and are variably responsible for eczema(staphylococcus), psoriasis(streptococcus) and arthritis(streptococcus). The biofilm matrix consists of exopolysaccharides held together with microbial amyloid-like proteins, stabilized by DNA; the less viscous dextrin/more viscous dextran glue that eventually polymerize to a rock-solid plaque upon exclusion of water. Dextrin is formed upon the action of hexosaminidase(lysozyme) on peptidoglycan and is a feature of the mast cell as well as the spirochete, while dextran is made from sucrose by bacteria.
Spirochetes easily pass through the blood-brain barrier. The Toll-like receptor 2 activation, in response to the amyloid-like protein, curli, from the spirochete in biofilm, generates NF-kB(nuclear factor kappa beta) and TNF-alpha(tumor necrotic factor alpha) which are the first responders that attempt to kill microbes in the biofilm but won't penetrate the matrix. They damage the (nerve)tissue instead. NF-kB also activates secretase to generate amyloid-beta peptide, which is antimicrobial but still won't penetrate the plaque. NF-kB is a complex of pro-inflammatory transcription factors that regulates immunity and responds to stress and toxic ligands, cytokines and hormones, inflammasomes by generating cytokines. Increased cellular metabolism--as with peroxisome activators on vitamins D and A receptors--in its own right, generates stress and produces signaling molecules that trigger NF-kB activation.
The amyloid-DNA complex is strongly immunogenic and has been implicated in autoimmunity in susceptible individuals. The amyloid-antibody complex is more active on the nerve at stimulating the NMDA receptor to open membrane channels. In fact, without the antibody, amyloid is inhibitory on this receptor. Moreover, as nerves are damaged, decreased miRNA synthesis upregulates NMDA receptors. Amyloid binds to fibroblasts, and mast cell MHC 1 thus activating them. Once microbial amyloid attaches to fibroblasts, mast cells accumulate, and both are activated and co-activate each other.
The mechanism has been beautifully elucidated elsewhere as follows:
"This pathway derives from the MyD88 pathway activated by TLR 2. TNF-α, generated by TLR 2, in conjugation with TNF-α converting enzyme (TACE) becomes alpha secretase and splits amyloid precursor protein (APP) to make amyloid alpha. The NF-kB generated by the same MyD88 pathway, together with Aβ converting enzyme (BACE), activates beta and gamma secretases that cleave the APP. The APP then becomes Aβ and attacks the biofilm but cannot penetrate it. Consequently, it encompasses the biofilm and its buildup destroys the neurocircuitry of the brain".
"This is the very essence of autoimmunity, namely the body attacking itself; this occurs when the body’s own innate immune system produces TNF-α or Aβ and attacks the biofilm encasing the spirochetes. In the process of doing this, the surrounding tissue is destroyed instead. Such is the case with the biofilm produced by staphylococcus in eczema and streptococcus in psoriasis; these biofilms call forth the innate immune system and the whole process of tissue destruction is set in motion. The consequences of AD are much more dire however, because they lead to total destruction of the mind".
Mast cells degranulation causes the formation of simple sugars and dextrin from peptidoglycan. Auto-oxidation of sugar, lipid peroxidation and the lipoxygenase pathway yield highly reactive malonyldialdehyde which cross links proteins and forms amyloid proteins from native ones as a by-product of glycation. Amyloids and advanced products of lipid peroxidation(malonyldialdehyde) bind to the scavenger receptor, RAGE(receptor of advanced glycation end-product) which suggests a common moiety.
Amyloidisis is therefore a common feature of hyperglycemia and the mast cell does not only supply the reactive oxygen species but also provides the sugar to cross-link into the beta sheet for amyloid formation. The mast cell also carries out the cleavage into amyloid peptides. Both albumin and keratin are known targets, and the presence of the exo-polysaccharides in biofilm serves to enhance amyloidosis. Many other proteins, including Apo-proteins, form amyloids. Amyloids are antimicrobial. They generate free radicals, due to the presence of bound iron or zinc as the catalytic center and through the opening up of calcium channels by mass process upon lodging in the plasma membrane, by interference with the mitochondrial membrane and by activating the MNDA receptor. Amyloids, themselves, may form conducting membrane pores. They possess lipase activity, which action is facilitated by their binding to and sequestering calcium--which calcium normally inhibits lipase.
Glycolysis also produces pyruvate aldehyde which, like malonydialdehyde, is very reactive--another marker of inflammation--binds strongly to nerves and cross-links membrane and myelin lipids(neuropathy), cross-links proteins, thus damaging tissue, producing amyloid and causing insulin resistance. Ketone bodies, however, neutralize pyruvate aldehyde more than they form this very compound. So stress, inflammation and ineffective antibiotic treatment promote amyloid and biofilm formation and essentially promote neurodegeneration.
Activation of nerves leads to free radical formation, and the oxidation of dopamine to a product that prevents the breadown of misfolded proteins by scrambling endosomes. Both the oxidized dopamine and misfolded proteins, in turn, negatively impact the mitochondria to produce more free radicals. Amyloid plaque outside the nerves, toxic amyloid oligomers that form pores in various compartmental membranes, inclusion bodies and tangles, inside the nerves as a result of lack of adequate autophagy, are all hallmarks of Alzheimer's and Parkinson's neurodegenerative diseases. Nerves eventually die from lack of activity, through the process of apoptosis.
Dr. Oliver Verbe Birnso, MD.
Spirochetes easily pass through the blood-brain barrier. The Toll-like receptor 2 activation, in response to the amyloid-like protein, curli, from the spirochete in biofilm, generates NF-kB(nuclear factor kappa beta) and TNF-alpha(tumor necrotic factor alpha) which are the first responders that attempt to kill microbes in the biofilm but won't penetrate the matrix. They damage the (nerve)tissue instead. NF-kB also activates secretase to generate amyloid-beta peptide, which is antimicrobial but still won't penetrate the plaque. NF-kB is a complex of pro-inflammatory transcription factors that regulates immunity and responds to stress and toxic ligands, cytokines and hormones, inflammasomes by generating cytokines. Increased cellular metabolism--as with peroxisome activators on vitamins D and A receptors--in its own right, generates stress and produces signaling molecules that trigger NF-kB activation.
The amyloid-DNA complex is strongly immunogenic and has been implicated in autoimmunity in susceptible individuals. The amyloid-antibody complex is more active on the nerve at stimulating the NMDA receptor to open membrane channels. In fact, without the antibody, amyloid is inhibitory on this receptor. Moreover, as nerves are damaged, decreased miRNA synthesis upregulates NMDA receptors. Amyloid binds to fibroblasts, and mast cell MHC 1 thus activating them. Once microbial amyloid attaches to fibroblasts, mast cells accumulate, and both are activated and co-activate each other.
The mechanism has been beautifully elucidated elsewhere as follows:
"This pathway derives from the MyD88 pathway activated by TLR 2. TNF-α, generated by TLR 2, in conjugation with TNF-α converting enzyme (TACE) becomes alpha secretase and splits amyloid precursor protein (APP) to make amyloid alpha. The NF-kB generated by the same MyD88 pathway, together with Aβ converting enzyme (BACE), activates beta and gamma secretases that cleave the APP. The APP then becomes Aβ and attacks the biofilm but cannot penetrate it. Consequently, it encompasses the biofilm and its buildup destroys the neurocircuitry of the brain".
"This is the very essence of autoimmunity, namely the body attacking itself; this occurs when the body’s own innate immune system produces TNF-α or Aβ and attacks the biofilm encasing the spirochetes. In the process of doing this, the surrounding tissue is destroyed instead. Such is the case with the biofilm produced by staphylococcus in eczema and streptococcus in psoriasis; these biofilms call forth the innate immune system and the whole process of tissue destruction is set in motion. The consequences of AD are much more dire however, because they lead to total destruction of the mind".
Mast cells degranulation causes the formation of simple sugars and dextrin from peptidoglycan. Auto-oxidation of sugar, lipid peroxidation and the lipoxygenase pathway yield highly reactive malonyldialdehyde which cross links proteins and forms amyloid proteins from native ones as a by-product of glycation. Amyloids and advanced products of lipid peroxidation(malonyldialdehyde) bind to the scavenger receptor, RAGE(receptor of advanced glycation end-product) which suggests a common moiety.
Amyloidisis is therefore a common feature of hyperglycemia and the mast cell does not only supply the reactive oxygen species but also provides the sugar to cross-link into the beta sheet for amyloid formation. The mast cell also carries out the cleavage into amyloid peptides. Both albumin and keratin are known targets, and the presence of the exo-polysaccharides in biofilm serves to enhance amyloidosis. Many other proteins, including Apo-proteins, form amyloids. Amyloids are antimicrobial. They generate free radicals, due to the presence of bound iron or zinc as the catalytic center and through the opening up of calcium channels by mass process upon lodging in the plasma membrane, by interference with the mitochondrial membrane and by activating the MNDA receptor. Amyloids, themselves, may form conducting membrane pores. They possess lipase activity, which action is facilitated by their binding to and sequestering calcium--which calcium normally inhibits lipase.
Glycolysis also produces pyruvate aldehyde which, like malonydialdehyde, is very reactive--another marker of inflammation--binds strongly to nerves and cross-links membrane and myelin lipids(neuropathy), cross-links proteins, thus damaging tissue, producing amyloid and causing insulin resistance. Ketone bodies, however, neutralize pyruvate aldehyde more than they form this very compound. So stress, inflammation and ineffective antibiotic treatment promote amyloid and biofilm formation and essentially promote neurodegeneration.
Activation of nerves leads to free radical formation, and the oxidation of dopamine to a product that prevents the breadown of misfolded proteins by scrambling endosomes. Both the oxidized dopamine and misfolded proteins, in turn, negatively impact the mitochondria to produce more free radicals. Amyloid plaque outside the nerves, toxic amyloid oligomers that form pores in various compartmental membranes, inclusion bodies and tangles, inside the nerves as a result of lack of adequate autophagy, are all hallmarks of Alzheimer's and Parkinson's neurodegenerative diseases. Nerves eventually die from lack of activity, through the process of apoptosis.
Dr. Oliver Verbe Birnso, MD.
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