Intrathecal inflammation precedes development of Alzheimer's disease

[Guest guest]

J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.

Intrathecal inflammation precedes development of Alzheimer's disease.

Tarkowski E, sen N, Tarkowski A, Blennow K.

Department of Rheumatology, University of Goteborg, Goteborg,

Sweden. elisabeth.tarkowski@...

OBJECTIVES: To analyse the cerebrospinal fluid (CSF) values of the

proinflammatory cytokines, interleukin 1beta (IL1beta), tumour

necrosis factor alpha (TNFalpha), GM-CSF, of the anti-inflammatory

cytokine TGFbeta, of tau protein, a marker for neurodegeneration, and

of beta amyloid (Abeta), a protein involved in the formation of senile

plaques, in prospectively followed up patients with mild cognitive

impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha,

IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed using

ELISA in 56 patients with MCI who were followed up prospectively and

in 25 age matched, healthy controls. RESULTS: Patients with MCI

displayed significantly higher levels of TNFalpha and tau protein and

significantly lower levels of TGFbeta and Abeta compared with the

healthy controls. After nine months of follow up, 25 patients still

displayed MCI while the remaining 31 patients had progressed to

Alzheimer's disease (AD). Only MCI patients who progressed to AD at

follow up, showed significantly higher CSF levels of TNFalpha than

controls. In addition, reduced CSF-Abeta42 levels were only found in

MCI patients that progressed to AD, further supporting the notion that

disturbed metabolism of Abeta is an early finding in AD. CONCLUSIONS:

These results demonstrate increased production of the proinflammatory

cytokine, TNFalpha and decreased production of the anti-inflammatory

cytokine TGFbeta in patients with MCI at risk to develop AD,

suggesting a propensity towards inflammation in this patient group and

indicating that CNS inflammation is a early hallmark in the

pathogenesis of AD.

PMID: 12933918 [PubMed - indexed for MEDLINE]

[Guest guest]

A recent australian study looking carefully at the brain tissue

samples was motivated by the microcirculatory damage that is clearly

evident just before the plagues start forming.Blown blood vessels

are very common in major infections.. HAving cardiovascular problems

causes more than just blood pressure issues.IMO.

tony

>

>

>

> J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.

>

> Intrathecal inflammation precedes development of Alzheimer's

disease.

>

> Tarkowski E, sen N, Tarkowski A, Blennow K.

>

> Department of Rheumatology, University of Goteborg, Goteborg,

> Sweden. elisabeth.tarkowski@...

>

> OBJECTIVES: To analyse the cerebrospinal fluid (CSF) values of

the

> proinflammatory cytokines, interleukin 1beta (IL1beta), tumour

> necrosis factor alpha (TNFalpha), GM-CSF, of the anti-inflammatory

> cytokine TGFbeta, of tau protein, a marker for neurodegeneration,

and

> of beta amyloid (Abeta), a protein involved in the formation of

senile

> plaques, in prospectively followed up patients with mild cognitive

> impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha,

> IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed

using

> ELISA in 56 patients with MCI who were followed up prospectively

and

> in 25 age matched, healthy controls. RESULTS: Patients with MCI

> displayed significantly higher levels of TNFalpha and tau protein

and

> significantly lower levels of TGFbeta and Abeta compared with the

> healthy controls. After nine months of follow up, 25 patients still

> displayed MCI while the remaining 31 patients had progressed to

> Alzheimer's disease (AD). Only MCI patients who progressed to AD at

> follow up, showed significantly higher CSF levels of TNFalpha than

> controls. In addition, reduced CSF-Abeta42 levels were only found

in

> MCI patients that progressed to AD, further supporting the notion

that

> disturbed metabolism of Abeta is an early finding in AD.

CONCLUSIONS:

> These results demonstrate increased production of the

proinflammatory

> cytokine, TNFalpha and decreased production of the anti-

inflammatory

> cytokine TGFbeta in patients with MCI at risk to develop AD,

> suggesting a propensity towards inflammation in this patient group

and

> indicating that CNS inflammation is a early hallmark in the

> pathogenesis of AD.

>

> PMID: 12933918 [PubMed - indexed for MEDLINE]

>

[Guest guest]

Dear Tony

Message flagged

Regards

Windsor

[infections] Re: Intrathecal inflammation precedes

development of Alzheimer's disease

>

> A recent australian study looking carefully at the brain tissue

> samples was motivated by the microcirculatory damage that is clearly

> evident just before the plagues start forming.Blown blood vessels

> are very common in major infections.. HAving cardiovascular problems

> causes more than just blood pressure issues.IMO.

> tony

>

>

>

>

>

>

>

> >

> >

> >

> > J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.

> >

> > Intrathecal inflammation precedes development of Alzheimer's

> disease.

> >

> > Tarkowski E, sen N, Tarkowski A, Blennow K.

> >

> > Department of Rheumatology, University of Goteborg, Goteborg,

> > Sweden. elisabeth.tarkowski@...

> >

> > OBJECTIVES: To analyse the cerebrospinal fluid (CSF) values of

> the

> > proinflammatory cytokines, interleukin 1beta (IL1beta), tumour

> > necrosis factor alpha (TNFalpha), GM-CSF, of the anti-inflammatory

> > cytokine TGFbeta, of tau protein, a marker for neurodegeneration,

> and

> > of beta amyloid (Abeta), a protein involved in the formation of

> senile

> > plaques, in prospectively followed up patients with mild cognitive

> > impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha,

> > IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed

> using

> > ELISA in 56 patients with MCI who were followed up prospectively

> and

> > in 25 age matched, healthy controls. RESULTS: Patients with MCI

> > displayed significantly higher levels of TNFalpha and tau protein

> and

> > significantly lower levels of TGFbeta and Abeta compared with the

> > healthy controls. After nine months of follow up, 25 patients still

> > displayed MCI while the remaining 31 patients had progressed to

> > Alzheimer's disease (AD). Only MCI patients who progressed to AD at

> > follow up, showed significantly higher CSF levels of TNFalpha than

> > controls. In addition, reduced CSF-Abeta42 levels were only found

> in

> > MCI patients that progressed to AD, further supporting the notion

> that

> > disturbed metabolism of Abeta is an early finding in AD.

> CONCLUSIONS:

> > These results demonstrate increased production of the

> proinflammatory

> > cytokine, TNFalpha and decreased production of the anti-

> inflammatory

> > cytokine TGFbeta in patients with MCI at risk to develop AD,

> > suggesting a propensity towards inflammation in this patient group

> and

> > indicating that CNS inflammation is a early hallmark in the

> > pathogenesis of AD.

> >

> > PMID: 12933918 [PubMed - indexed for MEDLINE]

> >

>

>

>

>

>

>

>

>

[Guest guest]

'

I'll flag you back???? I didn't get any of that.

tony

> > >

> > >

> > >

> > > J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.

> > >

> > > Intrathecal inflammation precedes development of

Alzheimer's

> > disease.

> > >

> > > Tarkowski E, sen N, Tarkowski A, Blennow K.

> > >

> > > Department of Rheumatology, University of Goteborg,

Goteborg,

> > > Sweden. elisabeth.tarkowski@

> > >

> > > OBJECTIVES: To analyse the cerebrospinal fluid (CSF)

values of

> > the

> > > proinflammatory cytokines, interleukin 1beta (IL1beta), tumour

> > > necrosis factor alpha (TNFalpha), GM-CSF, of the anti-

inflammatory

> > > cytokine TGFbeta, of tau protein, a marker for

neurodegeneration,

> > and

> > > of beta amyloid (Abeta), a protein involved in the formation of

> > senile

> > > plaques, in prospectively followed up patients with mild

cognitive

> > > impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha,

> > > IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed

> > using

> > > ELISA in 56 patients with MCI who were followed up

prospectively

> > and

> > > in 25 age matched, healthy controls. RESULTS: Patients with MCI

> > > displayed significantly higher levels of TNFalpha and tau

protein

> > and

> > > significantly lower levels of TGFbeta and Abeta compared with

the

> > > healthy controls. After nine months of follow up, 25 patients

still

> > > displayed MCI while the remaining 31 patients had progressed to

> > > Alzheimer's disease (AD). Only MCI patients who progressed to

AD at

> > > follow up, showed significantly higher CSF levels of TNFalpha

than

> > > controls. In addition, reduced CSF-Abeta42 levels were only

found

> > in

> > > MCI patients that progressed to AD, further supporting the

notion

> > that

> > > disturbed metabolism of Abeta is an early finding in AD.

> > CONCLUSIONS:

> > > These results demonstrate increased production of the

> > proinflammatory

> > > cytokine, TNFalpha and decreased production of the anti-

> > inflammatory

> > > cytokine TGFbeta in patients with MCI at risk to develop AD,

> > > suggesting a propensity towards inflammation in this patient

group

> > and

> > > indicating that CNS inflammation is a early hallmark in the

> > > pathogenesis of AD.

> > >

> > > PMID: 12933918 [PubMed - indexed for MEDLINE]

> > >

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

Dear Tony

A significant reference worthy of in depth exploration, flagged so I won't

forget it

Regards

r

[infections] Re: Intrathecal inflammation precedes

development of Alzheimer's disease

> '

> I'll flag you back???? I didn't get any of that.

> tony

>

>

>

> > > >

> > > >

> > > >

> > > > J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.

> > > >

> > > > Intrathecal inflammation precedes development of

> Alzheimer's

> > > disease.

> > > >

> > > > Tarkowski E, sen N, Tarkowski A, Blennow K.

> > > >

> > > > Department of Rheumatology, University of Goteborg,

> Goteborg,

> > > > Sweden. elisabeth.tarkowski@

> > > >

> > > > OBJECTIVES: To analyse the cerebrospinal fluid (CSF)

> values of

> > > the

> > > > proinflammatory cytokines, interleukin 1beta (IL1beta), tumour

> > > > necrosis factor alpha (TNFalpha), GM-CSF, of the anti-

> inflammatory

> > > > cytokine TGFbeta, of tau protein, a marker for

> neurodegeneration,

> > > and

> > > > of beta amyloid (Abeta), a protein involved in the formation of

> > > senile

> > > > plaques, in prospectively followed up patients with mild

> cognitive

> > > > impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha,

> > > > IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed

> > > using

> > > > ELISA in 56 patients with MCI who were followed up

> prospectively

> > > and

> > > > in 25 age matched, healthy controls. RESULTS: Patients with MCI

> > > > displayed significantly higher levels of TNFalpha and tau

> protein

> > > and

> > > > significantly lower levels of TGFbeta and Abeta compared with

> the

> > > > healthy controls. After nine months of follow up, 25 patients

> still

> > > > displayed MCI while the remaining 31 patients had progressed to

> > > > Alzheimer's disease (AD). Only MCI patients who progressed to

> AD at

> > > > follow up, showed significantly higher CSF levels of TNFalpha

> than

> > > > controls. In addition, reduced CSF-Abeta42 levels were only

> found

> > > in

> > > > MCI patients that progressed to AD, further supporting the

> notion

> > > that

> > > > disturbed metabolism of Abeta is an early finding in AD.

> > > CONCLUSIONS:

> > > > These results demonstrate increased production of the

> > > proinflammatory

> > > > cytokine, TNFalpha and decreased production of the anti-

> > > inflammatory

> > > > cytokine TGFbeta in patients with MCI at risk to develop AD,

> > > > suggesting a propensity towards inflammation in this patient

> group

> > > and

> > > > indicating that CNS inflammation is a early hallmark in the

> > > > pathogenesis of AD.

> > > >

> > > > PMID: 12933918 [PubMed - indexed for MEDLINE]

> > > >

> > >

> > >

> > >

> > >

> > >

> > >

> > >

> > >

[Guest guest]

gotcha

> > > > >

> > > > >

> > > > >

> > > > > J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.

> > > > >

> > > > > Intrathecal inflammation precedes development of

> > Alzheimer's

> > > > disease.

> > > > >

> > > > > Tarkowski E, sen N, Tarkowski A, Blennow K.

> > > > >

> > > > > Department of Rheumatology, University of Goteborg,

> > Goteborg,

> > > > > Sweden. elisabeth.tarkowski@

> > > > >

> > > > > OBJECTIVES: To analyse the cerebrospinal fluid (CSF)

> > values of

> > > > the

> > > > > proinflammatory cytokines, interleukin 1beta (IL1beta),

tumour

> > > > > necrosis factor alpha (TNFalpha), GM-CSF, of the anti-

> > inflammatory

> > > > > cytokine TGFbeta, of tau protein, a marker for

> > neurodegeneration,

> > > > and

> > > > > of beta amyloid (Abeta), a protein involved in the

formation of

> > > > senile

> > > > > plaques, in prospectively followed up patients with mild

> > cognitive

> > > > > impairment (MCI). METHODS: Analyses of CSF levels of

TNFalpha,

> > > > > IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were

performed

> > > > using

> > > > > ELISA in 56 patients with MCI who were followed up

> > prospectively

> > > > and

> > > > > in 25 age matched, healthy controls. RESULTS: Patients

with MCI

> > > > > displayed significantly higher levels of TNFalpha and tau

> > protein

> > > > and

> > > > > significantly lower levels of TGFbeta and Abeta compared

with

> > the

> > > > > healthy controls. After nine months of follow up, 25

patients

> > still

> > > > > displayed MCI while the remaining 31 patients had

progressed to

> > > > > Alzheimer's disease (AD). Only MCI patients who progressed

to

> > AD at

> > > > > follow up, showed significantly higher CSF levels of

TNFalpha

> > than

> > > > > controls. In addition, reduced CSF-Abeta42 levels were only

> > found

> > > > in

> > > > > MCI patients that progressed to AD, further supporting the

> > notion

> > > > that

> > > > > disturbed metabolism of Abeta is an early finding in AD.

> > > > CONCLUSIONS:

> > > > > These results demonstrate increased production of the

> > > > proinflammatory

> > > > > cytokine, TNFalpha and decreased production of the anti-

> > > > inflammatory

> > > > > cytokine TGFbeta in patients with MCI at risk to develop

AD,

> > > > > suggesting a propensity towards inflammation in this

patient

> > group

> > > > and

> > > > > indicating that CNS inflammation is a early hallmark in the

> > > > > pathogenesis of AD.

> > > > >

> > > > > PMID: 12933918 [PubMed - indexed for MEDLINE]

> > > > >

> > > >

> > > >

> > > >

> > > >

> > > >

> > > >

> > > >

> > > >