Alzheimer's disease

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Alzheimer's disease

Cpn & Alzheimer's-- nice description of Balin's work

This may have been noted before, but a nice summary of Balin's work on Chlamydia pneumoniae and Alzheimer's. Note his discussion of the need for using multple measures (up to 15) and different methodologies in trying to detect a very difficult to detect organism:

http://www.tangledneuron.info/the_tangled_neuron/2007/06/chlamydia-pneum.html<

my dad's alzhiemer's-doctor in Nashville

Hey's folks -ain't it funny how God works. I started on this path for my wife's CFSi beginning with possible Viral agents(Shell start supplementsi/naci nov 1.) then i linked up here after labs where negative for all but CPNi and i found this place. Now my dad's(ALZ dxi 8mos) neuroi is sending him to Nashville (home of Vanderbilt U) to see a specialist in the treatment of CPn. My mom just told me -don't have a name or backgrouund yet. I'll probably be driving him up from Pensacola FL for his appt Dec 1- I hope to take my wife also if I can get her an appt. More to come-thanks lwbell

my dad's alzhiemer's-doctor in Nashville

Hey's folks -ain't it funny how God works. I started on this path for my wife's CFSi beginning with possible Viral agents(Shell start supplementsi/naci nov 1.) then i linked up here after labs where negative for all but CPNi and i found this place. Now my dad's(ALZ dxi 8mos) neuroi is sending him to Nashville (home of Vanderbilt U) to see a specialist in the treatment of CPn. My mom just told me -don't have a name or backgrouund yet. I'll probably be driving him up from Pensacola FL for his appt Dec 1- I hope to take my wife also if I can get her an appt. More to come-thanks lwbell

Anyone experienced with treating Alzhiemers with the CAP?

Is any body out there doing CAPi for Alzhiemer's? I am having my dad do the Chlamydial Species Differentation test and hoping for a positive titer. He was diagnosed with Alzheimer's about a year ago. He was and remains a gifted physician and thinker. He is willing to give the protocolsi a 6month run but we are curious as to the expectation of the "Herx" and what we can anticipate as symptoms. Which Abxi crosses the BBBi and still is effective on the recticular body form. I know that flagyli crosses for the cryptic formi and doxyi gets the EBi.

My wife will be starting the protocol soon. CFSi 15yrs.

LWBELL

Alzheimers

My aunt has been diagnosed with Alzheimers. She is around 80 years old. Would CAPi work for my aunt? Or is it too late? I had a bad flare up of Cpni about 20 years ago that left me with brain fog, memory problems, and inability to more than one thing at a time. I felt like the cogs in my brain had sand in them. What is happening to my aunt could have happened to me.

Antibiotics useful against CPn which cross the blood brain barrier well?

I recently recovered some information from the former web site of Dr. Sririam pertaining to the usefullness of antibioticsi against Cpni and which ones will cross the blood brain barrier.  What I don't know is how accurate this information is or why some antibiotics that appear to be less effective at crossing the blood  brain barrier were chosen.  Why the latter question?  Because at least one of the doctors who have devised protocolsi did so with the specific objective of treating Multiple Sclerosisi, a neurological disease.  Crossing the blood brain barrier is critical in the success of such a treatment.

Chlamydophila (Chlamydia) pneumoniae infection of human astrocytes and microglia in culture displays an active, rather than a pe

Am J Med Sci. 2006 Oct;332(4):168-74. Chlamydophila (Chlamydia) pneumoniae infection of human astrocytes and microglia in culture displays an active, rather than a persistent, phenotype.Dreses-Werringloer U, Gérard HC, Whittum-Hudson JA, Hudson AP. Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

Essential Observations by Dr. Charles Stratton on Chlamydia Pneumoniae Infection and Disease

I am very excited to present the following article that summarizes Dr. Stratton's recent observations on Chlamydia pneumoniae infection. Putting it together has contributed greatly to my own understanding of Cpni as well as to my appreciation of Dr. Stratton's generosity with his time, and his great depth of knowledge of this area. Thanks to him for his contribution.

Jim K

Recent observations by Dr

Recent observations by Dr. Charles Strattoni on Chlamydia Pneumoniae (Cpn) Infection

Chlamydia pneumoniae infection of brain cells

This pre-publication abstract is a remarkable piece of laboratory work. It strengthens the case for Cpni infection especially in MSi and Alzheimer's, and other brain diseasesi.

The two findings I've underlined which seem to have espeical importance is (1) the sensitivity of neuronal cells to infection, as big producers of EB'si, and their particular sensitivity to necrosisi (tissue death); and (2) the finding in microglial cells that they resist active replicating infection but appear to be potential reservoirs for persistant Cpn.

  Neurobiol Aging. 2006 Apr 16; [Epub ahead of print]

Chlamydia pneumoniae infection of brain cells: An in vitro study.

Boelen E, Steinbusch HW, van der Ven AJ, Grauls G, Bruggeman CA, Stassen FR.

Department of Medical Microbiology, CARIM (Cardiovascular Research Institute Maastricht), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Department of Cellular Neuroscience, EURON (European Graduate School of Neurosciences), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.

Inspired by the suggested associations between neurological diseases and infectionsi, we determined the susceptibility of brain cells to Chlamydia pneumoniae (Cpn). Murine astrocytei (C8D1A), neuronal (NB41A3) and microglial (BV-2) cell lines were inoculated with Cpn. Infection was established by immunofluorescence and real-time PCRi at various time points. Productive infection was assessed by transferring medium of infected cells to a detection layer. Finally, apoptosisi and necrosis post-infection was determined. Our data demonstrate that the neuronal cell line is highly sensitive to Cpn, produces viable progeny and is prone to die after infection by necrosis. Cpn tropism was similar in an astrocyte cell line, apart from the higher production of extracellular Cpn and less pronounced necrosis. In contrast, the microglial cell line is highly resistant to Cpn as the immunohistochemical signs almost completely disappeared after 24h. Nevertheless, significant Cpn DNA amounts could be detected, suggesting Cpn persistencei. Low viable progeny and hardly any necrotic microglial cells were observed. Further research is warranted to determine whether these cell types show the same sensitivity to Cpn in an in vivo setting.

PMID: 16621171 [PubMed - as supplied by publisher]

Brian Balin's Research on Cpn in Alzheimer's Disease

Brian Balin has done a remarkable job of pursuing a consistent line of research looking at Chlamydia Pneumoniae as a causal source or co-factor in Alzheimer's disease.

Information about Dr. Balin can be found at this link.<

Comments he has made about his research can be found at this link<. Included is a comment he made which is very reminiscent of Dr. Sriram's answer's to negative studies by other researchers, noting that he, like Sriram, used frozen brain sections and found Cpni DNA, whereas the other researchers used formalin preserved sections and did not find Cpn evidence.

Diseases associated with Cpn: the exhaustive list

I have culled from Mitchell & Stratton patent #6,884,784 an exhaustive list of diseasesi where Cpni has been implicated as a possible cause or co-factor (reference: Mitchell & Stratton patent #6,884,784):

Diseases where an association has been discovered between chronic Chlamydia infection of body fluids and/or tissues with several disease syndromes of previously unknown etiology in humans which respond to unique antichlamydial regimens include:

Editorial comment: Strong findings from their research. If you have any of these it suggests to me that at least an empirical course of the combination antibiotic therapy is strongly indicated, with or without serologyi.


Multiple Sclerosis (MSi)
Rheumatoid Arthritis (RA)
Inflammatory Bowel Diseasei (IBD)
Interstitial Cystitisi (IC)
Fibromyalgiai (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndromei (CFSi).

NAC in neurodegenerative diseases

http://www.sciencedaily.com/releases/2005/12/051219173902.htm< has an interesting article that includes info on the protective effect of NAC in neurodegenerative disease.

The load of Chlamydia pneumoniae in the Alzheimer's brain varies with APOE genotype.

Microb Pathog. 2005 Jul 2; [Epub ahead of print]

The load of Chlamydia pneumoniae in the Alzheimer's brain varies with APOE genotype.
Gerard HC, Wildt KL, Whittum-Hudson JA, Lai Z, Ager J, Hudson AP.
Department of Immunology and Microbiology, Wayne State University School of Medicine, Gordon H. Scott Hall, 540 East Canfield Avenue, Detroit, MI 48201, USA.
Studies from this laboratory have indicated that the intracellulari eubacterial respiratory pathogen Chlamydophila (Chlamydia) pneumoniae is commonly found in brain regions displaying characteristic neuropathology in patients with late-onset Alzheimer's disease (AD) but not in congruent samples from non-AD control individuals. In later work, we provided evidence suggesting that some relationship exists between the APOE epsilon4 gene product and the pathobiology of this organism. In the present report, in situ hybridization analyses indicated that the number of C. pneumoniae-infected cells in affected brain regions of epsilon4-bearing AD patients was higher overall than that in congruent brain regions from AD patients lacking that allele. Quantitative real-time PCRi analyses of AD brain tissue samples demonstrated that actual bacterial burden in those samples varied over several orders of magnitude, but that samples from epsilon4-bearing patients did have significantly higher bacterial loads than did congruent samples from patients without the allele (ANOVA, p<0.05). These results may explain in part the observations that epsilon4-bearing individuals have a higher risk of developing AD, and that such patients progress more rapidly to cognitive dysfunction than do individuals lacking this allele.

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