Lyme-CFS Spinal Fluid Proteomes Lecture 5/26

[Guest guest]

--- lecture 5/26, Tustin, CA by author of Distinct Cerebrospinal

Fluid Proteomes Differentiate Post-Treatment

Date: Thu, 17 May 2012 21:32:56 -0700

From: Nava Grutman <2navale@...>

<melillo3@...>

One of the authors of

Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme

Disease from Chronic Fatigue Syndrome.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017287

will speak on Saturday, May 26, 2012 at

Tustin Library, 345 Main Street, Tustin, California 92780

As soon as the library books the exact time, I will repost, and one can

check their Calendar of Events webpage at:

http://web.ocpl.org/events/?b=Tustin

The speaker / author is

Jonas Bergquist, Department of Physical and Analytical Chemistry,

Uppsala University, Uppsala, Sweden

Schutzer SE, Angel TE, Liu T, Schepmoes AA, Clauss TR, Adkins JN, Camp

DG, Holland BK, *Bergquist J*, Coyle PK, RD, Fallon BA, Natelson

BH. (2011) Distinct Cerebrospinal Fluid Proteomes Differentiate

Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. PLoS ONE

6(2): e17287. doi:10.1371/journal.pone.0017287

*Abstract

Background

*Neurologic Post Treatment Lyme disease (/nPTLS/) and Chronic Fatigue

(/CFS/) are syndromes of unknown etiology. They share features of

fatigue and cognitive dysfunction, making it difficult to differentiate

them. Unresolved is whether /nPTLS/ is a subset of /CFS/.

*Methods and Principal Findings

*Pooled cerebrospinal fluid (CSF) samples from /nPTLS patients/, /CFS/

patients, and healthy volunteers were comprehensively analyzed using

high-resolution mass spectrometry (MS), coupled with immunoaffinity

depletion methods to reduce protein-masking by abundant proteins.

Individual patient and healthy control CSF samples were analyzed

directly employing a MS-based label-free quantitative proteomics

approach. We found that both groups, and individuals within the groups,

could be distinguished from each other and normals based on their

specific CSF proteins (p<0.01). /CFS/ (n = 43) had 2,783 non-redundant

proteins, /nPTLS/ (n = 25) contained 2,768 proteins, and healthy normals

had 2,630 proteins. Preliminary pathway analysis demonstrated that the

data could be useful for hypothesis generation on the pathogenetic

mechanisms underlying these two related syndromes.

*Conclusions

*/nPTLS/ and /CFS/ have distinguishing CSF protein complements. Each

condition has a number of CSF proteins that can be useful in providing

candidates for future validation studies and insights on the respective

mechanisms of pathogenesis. Distinguishing /nPTLS/ and /CFS/ permits

more focused study of each condition, and can lead to novel diagnostics

and therapeutic interventions.

Priscilla Hall, MD, MEd, AAFP

Santa Ana, CA