Re: alzheimer Cpn group strikes back

[Guest guest]

By the way they also in recent years induced Alzheimer lesions in mice

by infecting them with Cpn, that really seems to be a coup.

[Guest guest]

Super cool and freaky.

> Hot off the press. These are the workers who had their late-1990s

> finding of Cpn in all-but-one Alzheimer brain disconfirmed by like

3

> other groups. They now report, using real-time PCR, that Cpn loads

> in Alzheimer lesions contain 1,000 to above one BILLION organisms

> per 50 mg of lesioned brain. Thats a million-fold difference in

> bacterial load. Sounds almost crazy, but its important to recall

> that inflammatory responses are by no means a linear function of

> pathogen density; perhaps this could be particularly true in

> immunoprivelaged tissues like the brain. Even so I'd be a lil more

> comfortable with some good old fashioned quantitative

> immunomicroscopy.

>

> They also found that the load correlated positively with the

> presence of an Alzheimer-associated allele (p < 0.05, ie not a

> tremendously robust correlation).

>

> J Miklossy reported ~2000 borreliae /mL brain in Alzheimers a

decade

> ago and this was also disconfirmed (R M(a?)cLaughlin).

>

> ============================================================

>

> Microb Pathog. 2005 Jul-Aug;39(1-2):19-26. Related Articles,

Links

>

>

> 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. Hall, 540 East Canfield

Avenue,

> Detroit, MI 48201, USA.

>

> Studies from this laboratory have indicated that the intracellular

> 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

> PCR 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.

>

> PMID: 15998578 [PubMed - in process]

[Guest guest]

The disconfirmation by other groups drives me nuts. I dont know what

to think. Then theres Judit Miklossy's borrelia. What does it all mean?

A billion chlamydiae works out to a quarter milligram of the bastards;

that sounds like a do-able amount for 50 mg of lesioned brain.

Assumptions: brain and bacteria both have the density of water (close

enough), a chlamydia equals a 0.5-um cube.

By the way these were mostly in astroglia and microglia.

<jenbooks13@h...> wrote:

> Super cool and freaky.

[Guest guest]

Miklossy's work has not been replicated plus she did not say it was

borrelia...it was intriguing preliminary data but doesn't leave us

with much...

> > Super cool and freaky.

[Guest guest]

<jenbooks13@h...> wrote:

> Miklossy's work has not been replicated plus she did not say it was

> borrelia...it was intriguing preliminary data but doesn't leave us

> with much...

The work on neither Cpn, nor Bb in AD has been replicated (except by

the same workers); indeed it has all been explicitly disconfirmed by

others.

Miklossy did identify her organisms as Bb: " Positive identification of

the agent as Borrelia burgdorferi sensu stricto was based on genetic

and molecular analyses. Borrelia antigens and genes were co-localized

with beta-amyloid deposits in these AD cases. [PMID: 15665404] "