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Welcome to CNTN

Welcome to the California NeuroAIDS Tissue Network


MISSION
The California NeuroAIDS Tissue Network (CNTN) is a research resource based at the University of California, San Diego, sponsored by the U.S. National Institute of Mental health, National Institutes of Health (NIMH/NIH Award Number U01MH083506). CNTN acquires and makes available well-characterized tissues from individuals who have Central Nervous System involvement with Human Immunodeficiency Virus (HIV).

ABOUT
CNTN is an organization of research scientists and clinicians dedicated to the study of neurological and psychological impairment in HIV infection. CNTN includes researchers from the Harbor-UCLA Research and Education Institute, Torrance, the University of California, San Diego, and the University of California, Irvine. Funded by the National Institute of Mental Health, CNTN is on of four sites participating in the larger National NeuroAIDS Tissue Consortium. Together, these researchers use their shared knowledge and resources to develop uniform methods for studying HIV‑affected populations with neurological disorders.

 


Requests for Research Specimens

The National NeuroAIDS Tissue Consortium (NNTC) coordinates requests for HIV+ tissues, fluids, and data from NeuroAIDS researchers across the globe. To submit a request through the NNTC, please visit www.nntc.org.

For researchers interested in submitting a request to CNTN directly, click here to download our request form.

 

Eric Tatro presents at ISNV and receives travel award!!

The 11th International Symposium on NeuroVirology (ISNV) will start on May 29, 2012 in New York, NY. The overall goal of the meeting is to provide investigators working in the field of neurovirology and related areas with leading edge information so that new preventative and therapeutic strategies effective against neurologic diseases associated with prions, HIV, and other viral and non-viral pathogens can be identified.

Read more...
 

CNTN Investigators Present at CROI 2012!

The following were presented by CNTN investigators at the 19th Conference on Retroviruses and Opportunistic Infections in Seattle, Washington on March 5-8, 2012.

  1. Nathamu S, Adame A, Dumoap W, Gouaux B, Moore D, Masliah E, Singh K, and the HNRC Group. (2012). Lectin complement pathway activation is linked to immune complex deposition in HIV encephalitis.
  2. Nathamu S, Adame A, Dumaop W, Gouaux B, Moore D, Masliah, E, Singh K, and the HNRC Group. (2012). Increased expression of complement receptor 2 and ligand C3 deposition in HIV encephalitis: A potential link to innate and adaptive immune responses in NeuroAIDS.
  3. Perez-Santiago J, Plongthongkum N, Letendre S, Ellis R, Gouaux B, Moore D, LeBlanc S, Rajagopal N, Zhang K, Woelk C. (2012). DNA methylation correlates with neurological decline in HIV-infected individuals.

Click Here for Posters to view for select abstracts above.  A Poster is available for viewing if there is a link in the left hand column next to the abstract title

 

Josue Perez-Santiago Awarded CROI 2012 Young Investigator Award Using CNTN Data!

The 19th Conference on Retroviruses and Opportunistic Infections in Seattle, Washington on March 5-8, 2012 awards travel expenses to promising young investigators.  Josue Perez-Santiago becomes the second HNRP affiliated investigator to win such an award (Dr. David Croteau previously won this award). The winning abstract is included below and utilized CNTN study generated data.  The results suggest that methylation profiles could be used as a prognostic as well as a diagnostic tool for neurocognitive decline in HIV infection. DNA methylation may provide a rich source for biomarker development since, in addition to the repression of promoter activity, methylation can also indicate the repression of distal regulatory elements.

Perez-Santiago J, Plongthongkum N, Letendre S, Ellis R, Gouaux B, Moore D, LeBlanc S, Rajagopal N, Zhang K, Woelk C. (2012). DNA methylation correlates with neurological decline in HIV-infected individuals.

 
 

Sponsored by NIH/NIMH/NINDS U01MH083506

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