Re: Ineffective phagocytosis of amyloid-beta in Alzheimer's

[Guest guest]

Could it be that this is a result of brain-immune

cells being infected with chlamydia pneumoniae? As an

obligate parasite, Cpn hijacks the the ATP machinery

of cells it infects, including monocytes, macrophages,

lymphocytes, etc., rendering them less functional and

" ineffective. " Since it's been implicated in

Alzheimers and found in Alzheimers plaques, it could

be a culprit. Makes you wonder why it isn't even

mentioned or controlled for in a study like this.

By the bye, we are getting a nice collection of

studies referenced at the www.cpnhelp.org site. While

we will get them better organized as the weeks go on,

I'd say it's open for business. You can help spread

the word by getting it out to other infections or

disease sites you know where it might be relevant.

Jim

Date: Mon, 05 Sep 2005 17:52:57 -0000

From: " Schaafsma " <compucruz@...>

Subject: " Ineffective phagocytosis of amyloid-beta " in

Alzheimer's

I would very much like to see the full text of this

article!

J Alzheimers Dis. 2005 Jun;7(3):221-32; discussion

255-62.

Ineffective phagocytosis of amyloid-beta by

macrophages of

Alzheimer's disease patients.

Fiala M, Lin J, Ringman J, Kermani-Arab V, Tsao G,

Patel A,

Lossinsky AS, Graves MC, Gustavson A, Sayre J, Sofroni

E, Suarez T,

Chiappelli F, Bernard G.

Department of Medicine, Greater LA VA Medical Center

and UCLA School

of Medicine, Los Angeles, CA 90095, USA.

fiala@...

The defective clearance of amyloid-beta (Abeta) in the

brain of

Alzheimer's disease (AD) patients is unexplained. The

immunohistochemical studies of the frontal lobe and

hippocampus show

perivascular and intraplaque infiltration by

blood-borne macrophages

containing intracellular Abeta but only inefficient

clearance of

beta deposits. Neurons and neuronal nuclei,

respectively, express

interleukin-1beta and the chemokine RANTES, which

could induce the

inflammatory cell infiltration. To clarify the

pathophysiology of

beta clearance, we examined Abeta phagocytosis by

monocytes and

macrophages isolated from the blood of age-matched

patients and

controls.

Control monocytes display excellent differentiation

into macrophages

and intracellular phagocytosis of Abeta followed by

beta degradation

or export. AD monocytes show poor differentiation and

only surface

uptake of Abeta and suffer apoptosis. HLA DR and

cyclooxygenase-2

are abnormally expressed on neutrophils and monocytes

of AD

patients. AD patients have higher levels of

intracellular cytokines

compared to controls. Thus Abeta clearance is not

restricted to

brain microglia and involves systemic innate immune

responses. In

AD, however, macrophage phagocytosis is defective,

which may elicit

compensatory response by the adaptive immune system.

PMID: 16006665 [PubMed - in process]

[Guest guest]

Macrophages are one of a group of multifunctional cells ..If the pathogen succeeds in promoting a runaway inflammatory response as part of a IS avoidance strategy. Then the role of the Macros & co gets confused.......It's a matter of he who shouts loudest gets the macrophage of choice ..cytokines either summons up .an engulphing attacking Macro or a wound response Macro promoting the laying down of fibrin ..it's either or ..not both together ...It could be viewed as a factor or a cause in disease , in most cases it's a factor.

It's the basis of s big push second paper.....A normal state ..with accelerators taking the bodies response "out of normal" & brakes [ARB's for one] bringing the out of control process back into the normal range...If you recall there are basically three such sates ..with various accelerators & brakes for each one ...Inflammation being the dominant accelerator ....

"Ineffective phagocytosis of amyloid-beta" inAlzheimer'sI would very much like to see the full text of thisarticle!J Alzheimers Dis. 2005 Jun;7(3):221-32; discussion255-62. Ineffective phagocytosis of amyloid-beta bymacrophages of Alzheimer's disease patients.Fiala M, Lin J, Ringman J, Kermani-Arab V, Tsao G,Patel A, Lossinsky AS, Graves MC, Gustavson A, Sayre J, SofroniE, Suarez T, Chiappelli F, Bernard G.Department of Medicine, Greater LA VA Medical Centerand UCLA School of Medicine, Los Angeles, CA 90095, USA.fiala@...The defective clearance of amyloid-beta (Abeta) in thebrain of Alzheimer's disease (AD) patients is unexplained. The immunohistochemical studies of the frontal lobe andhippocampus show perivascular and intraplaque infiltration byblood-borne macrophages containing intracellular Abeta but only inefficientclearance of beta deposits. Neurons and neuronal nuclei,respectively, express interleukin-1beta and the chemokine RANTES, whichcould induce the inflammatory cell infiltration. To clarify thepathophysiology of beta clearance, we examined Abeta phagocytosis bymonocytes and macrophages isolated from the blood of age-matchedpatients and controls. Control monocytes display excellent differentiationinto macrophages and intracellular phagocytosis of Abeta followed bybeta degradation or export. AD monocytes show poor differentiation andonly surface uptake of Abeta and suffer apoptosis. HLA DR andcyclooxygenase-2 are abnormally expressed on neutrophils and monocytesof AD patients. AD patients have higher levels ofintracellular cytokines compared to controls. Thus Abeta clearance is notrestricted to brain microglia and involves systemic innate immuneresponses. In AD, however, macrophage phagocytosis is defective,which may elicit compensatory response by the adaptive immune system.PMID: 16006665 [PubMed - in process]

[Guest guest]

's got the support of all kinds of big name scientists, and his

arb/cancer stuff was breakthrough research scrutinized by numerous

scientists before publication. When he did publish it, it got a lot of

well deserved attention. He's one smart guy.

penny

> Where's you know WHO in all this?

> Is by-passing him working alone- or working with him?

> Barb

>

/09/2005