2005 | 2004 | 2003 | 2002 | 2001

Alarcon M, Yonan AL, Gilliam TC, Cantor RM, Geschwind DH.
Quantitative genome scan and Ordered-Subsets Analysis of autism endophenotypes support language QTLs.
PMID: 15824743
Mol Psychiatry. 2005 Apr 12

Cantor RM, Kono N, Duvall JA, Alvarez-Retuerto A, Stone JL, Alarcon M, Nelson SF, Geschwind DH.
Replication of Autism Linkage: Fine-Mapping Peak at 17q21.
PMID: 15806440
Am J Hum Genet. 2005 Apr 1;76(6)

Bartlett CW, Gharani N, Millonig JH, Brzustowicz LM.
Three autism candidate genes: a synthesis of human genetic analysis with other disciplines.
PMID: 15749247
Int J Dev Neurosci. 2005 Apr-May;23(2-3):221-34.

Bartlett CW, Goedken R, Vieland VJ.
Effects of Updating Linkage Evidence across Subsets of Data: Reanalysis of the Autism Genetic Resource Exchange Data Set.
PMID: 15729670
Am J Hum Genet. 2005 Feb 23;76(4)

Summary by AGRE's Researcher Liaison Vlad Kustanovich Ph.D. :

Results of autism genetic linkage studies by research groups worldwide have been difficult to interpret. In an effort to reach more conclusive results, scientists have begun using larger sample sizes in their studies. However, we have found that simply increasing the sample size of disparate collections for a single analysis may not have been as effective as we had expected.

In this new study, using family samples from the Autism Genetic Resource Exchange, researchers applied what is known as the posterier probability of linkage (PPL). This method was designed specifically to analyze multiple heterogeneous data samples to update the PPL over these samples.

The results were remarkable. Their findings now indicate a substantial likelihood of a link to chromosome 1, which previously had been overlooked. The results also provided further characterization of the possible parent-of-origin effects of the 17q11 locus.

This shift in analysis strategy enables scientists to dramatically improve overall conclusions determined in a linkage study.

McCauley JL, Li C, Jiang L, Olson LM, Crockett G, Gainer K, Folstein SE, Haines JL, Sutcliffe JS.
Genome-wide and Ordered-Subset linkage analyses provide support for autism loci on 17q and 19p with evidence of phenotypic and interlocus genetic correlates.
PMID:15647115
BMC Med Genet. 2005 Jan 12;6(1):1

Summary by AGRE's Researcher Liaison Vlad Kustanovich Ph.D. :

Many geneticists believe that autism is caused by an interaction of several genetic and possibly environmental factors.

A group of scientists, led by Dr. James Sutcliffe, used genetic information from AGRE families, as well as families participating in the Vanderbilt and Tuft studies, to look at the involvement of multiple genetic regions of susceptibility in contributing to specific "TRAITS" of autistic behavior. The data for these traits were extracted from the Autism Diagnostic Interview.

This approach helps researchers focus on the relationship between targeted gene regions and how their interaction may be a factor in autism. The researchers examined the genetic evidence in families with autism in combination with some additional specific "TRAITS" (low levels of language, repetitive behaviors, etc.)

These researchers discovered strong evidence that linked autism to the interaction of specific genetic regions on 19q and 17q, as well as 7q and 5q. These regions are important because they were previously identified as being important in autism.