The Alzheimer’s Disease Neuroimaging Initiative announced this week that its genomewide analysis is 95 percent complete. ADNI is a collaborative project studying more than 800 people who have AD, mild cognitive impairment, or neither in the case of control subjects (see ARF related news story). The multisite, $60 million project, funded by the National Institutes of Health and the private sector, aims to integrate brain imaging, biochemistry, neuropsychological assessment, and genetics to identify biomarkers to diagnose and track the development of AD.

“It’s a landmark dataset that I think is likely to have a very high impact,” said Andrew Saykin of the Indiana University School of Medicine, leader of the ADNI genetic team. The genetics portion of the study read more than 620,000 DNA markers, and scientists will be able to look for genetic correlations with all of ADNI’s other data. “There’s an incredibly rich phenotype…much more than the presence or absence of disease,” Saykin said. The ADNI data will be available online to qualified scientists. Saykin expects to complete the last samples within two or three months, and to present preliminary results at the International Conference on Alzheimer’s Disease this summer.

Also this week, ADNI scientists published results from cerebrospinal fluid analyses of 416 subjects in the 18 March Annals of Neurology online. The authors define threshold values for cerebrospinal amyloid-β and tau that are associated with disease, but, equally importantly, they present standardized methods for collecting and storing samples and for measuring protein levels. Because ADNI encompasses 59 centers, an essential part of the project is to make sure everyone does the same experiments the same way. “The need for standardization is great, because we’re dealing with small changes over time,” said first author Leslie Shaw of the University of Pennsylvania in Philadelphia. “We hope this will benefit future clinical trials as a standard setting.”—Amber Dance


  1. I wonder whether the segregation power of this assay would be further strengthened if a marker of gliosis (GFAP, Iba1) or neuronal cell lysis (neurofilament) were added to the set.

    View all comments by Florian Muller

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Other Citations

  1. ARF related news story

External Citations

  1. ADNI data

Further Reading


  1. . Beta amyloid in Alzheimer's disease: increased deposition in brain is reflected in reduced concentration in cerebrospinal fluid. Biol Psychiatry. 2009 Jun 1;65(11):927-34. PubMed.
  2. . Analytic methods for factors, dimensions and endpoints in clinical trials for Alzheimer's disease. J Nutr Health Aging. 2009 Mar;13(3):249-55. PubMed.
  3. . Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain. Arch Neurol. 2009 Mar;66(3):382-9. PubMed.
  4. . Increased TDP-43 protein in cerebrospinal fluid of patients with amyotrophic lateral sclerosis. Acta Neuropathol. 2009 Jan;117(1):55-62. PubMed.
  5. . Visual rating system for assessing magnetic resonance images: a tool in the diagnosis of mild cognitive impairment and Alzheimer disease. J Comput Assist Tomogr. 2009 Jan-Feb;33(1):73-8. PubMed.
  6. . Baseline and longitudinal patterns of brain atrophy in MCI patients, and their use in prediction of short-term conversion to AD: results from ADNI. Neuroimage. 2009 Feb 15;44(4):1415-22. PubMed.

Primary Papers

  1. . Cerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects. Ann Neurol. 2009 Apr;65(4):403-13. PubMed.