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The second gene, NEFH, was identified in 1994, followed by SETX in 1998, ALS2 in 2001, DCTN1 in 2003, and CHMP2B in 2006. All of these genes are fairly rare; the next major ALS gene, TARDBP, was identified in 2008 and accounts for 4% of fALS and 1% of sALS. FUS was identified in 2009 and is seen in 4% of fALS and 1% of sALS.
Many animals have been used over the years to study ALS and to search for a potential therapy. [1] The animal models can be C. elegans which has only 959 cells with simple structure, and known gene code. [4]
There have been calls in the research community to routinely counsel and test all diagnosed ALS patients for familial ALS, [70] particularly as there is now a licensed gene therapy specifically targeted to carriers of SOD-1 ALS. A shortage of genetic counselors and limited clinical capacity to see such at-risk individuals makes this challenging ...
The Foundation's first therapy concept was to replace EAAT2 protein using gene therapy. [2] [4] In 2004, the Foundation moved to a 16,000-square-foot (1,500 m 2) location in Cambridge, Massachusetts with an in-house lab. ALS TDF constructed a biosafety level 2 lab in 2005, allowing for the expansion of "gene therapy and cell-based treatment ...
Bryan J. Traynor is a neurologist and a senior investigator at the National Institute on Aging, and an adjunct professor at Johns Hopkins University. [1] Dr. Traynor studies the genetics of human neurological conditions such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
The institute's initial approach focused on gene therapy and stem cells and ALS TDI was the first to publish on the safety of the use of stem cells in ALS patients. [3] ALS TDI then pioneered a novel high-throughput in-vivo validation program [ 4 ] that tested more treatments in preclinical studies than all other labs combined and led to two ...
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