Post by Niels on Sept 3, 2008 18:06:34 GMT -5
Everybody knows that alzheimer's is one of those bogus
made-up diseases based on lyme denialism -- a disease that
doesn't exist, used to give drugs that reduce symptoms, don't cure, are addictive, and must be taken for the shortened lifespan of the patient.
Fortunately, there's been some truths allowed to poke through about the fact that it's (along w/ autism) is really just lyme disease: linkinghub.elsevier.com/retrieve/pii/S0306987706001551
buckminster.physics.sunysb.edu/papers/InVitroBetaAmyloid.pdf
www.lymeinducedautism.com/images/TBILB_Autism.pdf
www.canlyme.com/alz.html
discoverandrecover.wordpress.com/2008/06/20/alzheimers-and-lyme-disease-a-series/
www.endowmentmed.org/pdf/updatelyme.pdf
www.ncbi.nlm.nih.gov/pubmed/16528463
tinyurl.com/65h8bf ( stanford.wellsphere.com/lyme-disease-article/m.s.,-parkinson%27s,-or-simply-lyme-disease?/116994 )
One article in particular of these stood out with some more
detailed description of these "amyloid plaques" in Alzheimer's Disease (AD):
* rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain
* Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury.
* an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques "cotton wool" type plaques, lack a central congophilic core structure
www.ncbi.nlm.nih.gov/pubmed/16675154
1: Med Hypotheses. 2006;67(3):592-600. Epub 2006 May 3.
Plaques of Alzheimer's disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete.
MacDonald AB.
St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA. inmacdonald@yahoo.com
Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded "plaques' in high density in brain tissue are emblematic of Alzheimer's disease (AD). Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed in plaques, amyloid is regularly represented by the "congophilic core" structure which is so named because the waxy amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques "cotton wool" type plaques, lack a central congophilic core structure). Furthermore, there is "plaque diversity" in Alzheimer's; small, medium and large plaques parallel variable cystic diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer's, is it possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis for Alzheimer's disease. In the "anatomy is destiny" model, cysts of borrelia are always round. Why then not accept roundness as a fundamental "structure determines function" argument for the answer to the mystery of why Alzheimer plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship. Parataxis tells us that what appears to be cause and effect in the couplet "amyloid plaque" merely by a proximity relationship may be "spurious causality" which is a cognitive dead end.
PMID: 16675154 [PubMed - indexed for MEDLINE]
A different article published at the same time discusses how amyloid plaques come about from borrelia spirochetes:
www.ncbi.nlm.nih.gov/pubmed/15894409
1: Neurobiol Aging. 2006 Feb;27(2):228-36.
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes.
Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K.
Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3. judmik@telus.net
The pathological hallmarks of Alzheimer's disease (AD) consist of beta-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased levels of beta-amyloid precursor protein (AbetaPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced.
made-up diseases based on lyme denialism -- a disease that
doesn't exist, used to give drugs that reduce symptoms, don't cure, are addictive, and must be taken for the shortened lifespan of the patient.
Fortunately, there's been some truths allowed to poke through about the fact that it's (along w/ autism) is really just lyme disease: linkinghub.elsevier.com/retrieve/pii/S0306987706001551
buckminster.physics.sunysb.edu/papers/InVitroBetaAmyloid.pdf
www.lymeinducedautism.com/images/TBILB_Autism.pdf
www.canlyme.com/alz.html
discoverandrecover.wordpress.com/2008/06/20/alzheimers-and-lyme-disease-a-series/
www.endowmentmed.org/pdf/updatelyme.pdf
www.ncbi.nlm.nih.gov/pubmed/16528463
tinyurl.com/65h8bf ( stanford.wellsphere.com/lyme-disease-article/m.s.,-parkinson%27s,-or-simply-lyme-disease?/116994 )
One article in particular of these stood out with some more
detailed description of these "amyloid plaques" in Alzheimer's Disease (AD):
* rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain
* Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury.
* an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques "cotton wool" type plaques, lack a central congophilic core structure
www.ncbi.nlm.nih.gov/pubmed/16675154
1: Med Hypotheses. 2006;67(3):592-600. Epub 2006 May 3.
Plaques of Alzheimer's disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete.
MacDonald AB.
St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA. inmacdonald@yahoo.com
Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded "plaques' in high density in brain tissue are emblematic of Alzheimer's disease (AD). Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed in plaques, amyloid is regularly represented by the "congophilic core" structure which is so named because the waxy amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques "cotton wool" type plaques, lack a central congophilic core structure). Furthermore, there is "plaque diversity" in Alzheimer's; small, medium and large plaques parallel variable cystic diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer's, is it possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis for Alzheimer's disease. In the "anatomy is destiny" model, cysts of borrelia are always round. Why then not accept roundness as a fundamental "structure determines function" argument for the answer to the mystery of why Alzheimer plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship. Parataxis tells us that what appears to be cause and effect in the couplet "amyloid plaque" merely by a proximity relationship may be "spurious causality" which is a cognitive dead end.
PMID: 16675154 [PubMed - indexed for MEDLINE]
A different article published at the same time discusses how amyloid plaques come about from borrelia spirochetes:
www.ncbi.nlm.nih.gov/pubmed/15894409
1: Neurobiol Aging. 2006 Feb;27(2):228-36.
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes.
Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K.
Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3. judmik@telus.net
The pathological hallmarks of Alzheimer's disease (AD) consist of beta-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased levels of beta-amyloid precursor protein (AbetaPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced.