alzheimer Cpn group strikes back

[Guest guest]

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).

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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]