Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
CSF phospho-tau correlates with behavioural decline and brain insoluble phospho-tau levels in a rat model of tauopathy.
Norbert Zilka; Miroslava Korenova; Branislav Kovacech; Khalid Iqbal; Michal Novak (Profiled Author: Iqbal, Khalid)
Institute of Neuroimmunology, Centre of Excellence for Alzheimer's Disease and Related Disorders, Slovak Academy of Sciences, Dubravska 9, 84510 Bratislava, Slovak Republic.
Acta neuropathologica 2010;119(6):679-87.
The aim of the present study was to identify the relationship between progressive neurobehavioural decline and phospho-tau levels (p-tau(181)) in the cerebrospinal fluid (CSF) and the brain in transgenic rats expressing human truncated tau protein. Behavioural analyses, as quantified using the NeuroScale scoring method, revealed that the transgenic rats fell into two main groups based on the baseline behavioural functioning: (1) mild neurobehavioural impairment (MNI, score 3.3-26) and (2) severe neurobehavioural impairment (SNI, score 36-44). SNI transgenic rats showed a significant increase in brain sarkosyl insoluble p-tau(181) when compared to their MNI counterparts. In order to determine whether CSF phospho-tau reflects the behavioural decline and increase in sarkosyl insoluble tau in the brain, p-tau(181) was measured in the CSF in a longitudinal study. The study showed a significant increase in CSF p-tau(181) during the progression of the disease from MNI to SNI. Moreover, increased levels of p-tau(181) in CSF correlated with an increase in the sarkosyl insoluble p-tau(181) levels in the brain. The increase in the CSF level of p-tau(181) during progressive behavioural decline suggests that it may represent a useful surrogate biomarker for preclinical drug development and a potential surrogate endpoint for clinical trials of disease-modifying therapy for Alzheimer's disease and related human tauopathies.
1 Originating Grant
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1.
IQBAL, KHALID
Subgroups of Alzheimer Disease
15 May 2007 - 30 April 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,630,946
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
IQBAL, KHALID
Abnormal Hyperphosphorylation of Tau
1 February 2001 - 30 April 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 3,687,819
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2.
IQBAL, KHALID
2 September 2011 - 30 June 2014
FOGARTY INTERNATIONAL CENTER
Total Funding: $ 70,352
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3.
HYMAN, BRADLEY T.
Anatomical Changes in Tau Transgenic Models
30 September 2004 - 31 August 2015
NATIONAL INSTITUTE ON AGING
Total Funding: $ 2,379,623
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