ResearchALS.org
is available for sale
About ResearchALS.org
Former two words, brandable domain representing Research ALS - the Alzheimer Research Forum, also known as the Alzforum, is an online research community dedicated to furthering research into Alzheimer's disease and related neurodegenerative disorders.
Exclusively on Odys Marketplace
$4,140
What's included:
Domain name ResearchALS.org
Become the new owner of the domain in less than 24 hours.
Complimentary Logo Design
Save time hiring a designer by using the existing high resolution original artwork, provided for free by Odys Global with your purchase.
Built-In SEO
Save tens of thousands of dollars and hundreds of hours of outreach by tapping into the existing authority backlink profile of the domain.
Free Ownership Transfer
Tech Expert Consulting
100% Secure Payments
Premium Aged Domain Value
Usually Seen In
Age
Traffic
SEO Metrics
Own this Domain in 3 Easy Steps
With Odys, buying domains is easy and safe. Your dream domain is just a few clicks away.
.1
Buy your Favorite Domain
Choose the domain you want, add it to your cart, and pay with your preferred method.
.2
Transfer it to your Registrar
Follow our instructions to transfer ownership from the current registrar to you.
.3
Get your Brand Assets
Download the available logos and brand assets and start building your dream website.
Trusted by the Top SEO Experts and Entrepreneurs
Rachel Parisi
★ ★ ★ ★ ★
I purchased another three aged domains from Odys in a seamless and painless transaction. John at Odys was super helpful! Odys is my only source for aged domains —you can trust their product.
Stefan
★ ★ ★ ★ ★
Odys is absolutely the best premium domain marketplace in the whole internet space. You will not go wrong with them.
Adam Smith
★ ★ ★ ★ ★
Great domains. Great to deal with. In this arena peace of mind can be difficult to come by, but I always have it with Odys and will continue to use them and recommend them to colleagues and clients.
Brett Helling
★ ★ ★ ★ ★
Great company. Very professional setup, communication, and workflows. I will definitely do business with Odys Global moving forward.
Larrian Gillespie Csi
★ ★ ★ ★ ★
I have bought 2 sites from Odys Global and they have both been of high quality with great backlinks. I have used one as the basis for creating a new site with a great DR and the other is a redirect with again high DR backlinks. Other sites I have looked through have low quality backlinks, mostly spam. I highly recommend this company for reliable sites.
Henry Fox
★ ★ ★ ★ ★
Great company!
Vijai Chandrasekaran
★ ★ ★ ★ ★
I’ve bought over 30 domains from Odys Global in the last two years and I was always very satisfied. Besides great quality, niche-specific auction domains, Alex also helped me a lot with SEO and marketing strategies. Auction domains are not cheap, but quality comes with a price. If you have the budget and a working strategy, these domains will make you serious money.
Keith
★ ★ ★ ★ ★
Earlier this year, I purchased an aged domain from Odys as part of a promo they’re running at the time. It was my first experience with buying an aged domain so I wanted to keep my spend low. I ended up getting a mid level DR domain for a good price. The domain had solid links from niche relevant high authority websites. I used the site as a 301 redirect to a blog I had recently started. Within a few weeks I enjoyed new traffic levels on my existing site. Happy to say that the Odys staff are friendly and helpful and they run a great business that is respected within the industry.
REVIEW ARTICLE
Design, power, and interpretation of studies in the standard murine model of ALS SEAN SCOTT1 , JANICE E. KRANZ1 , JEFF COLE1 , JOHN M. LINCECUM1 , KENNETH THOMPSON1 , NANCY KELLY1 , ALAN BOSTROM2 , JILL THEODOSS1 , BASHAR M. AL-NAKHALA1 , FERNANDO G. VIEIRA1 , JEYANTHI RAMASUBBU1 & JAMES A. HEYWOOD1 1 ALS Therapy Development Institute, Cambridge, Massachusetts, and 2 Department of Epidemiology and Biostatistics, University of California, San Francisco, USA Abstract Identification of SOD1 as the mutated protein in a significant subset of familial amyotrophic lateral sclerosis (FALS) cases has led to the generation of transgenic rodent models of autosomal dominant SOD1 FALS. Mice carrying 23 copies of the human SOD1G93A transgene are considered the standard model for FALS and ALS therapeutic studies. To date, there have been at least 50 publications describing therapeutic agents that extend the lifespan of this mouse. However, no therapeutic agent besides riluzole has shown corresponding clinical efficacy. We used computer modeling and statistical analysis of 5429 SOD1G93A mice from our efficacy studies to quantify the impact of several critical confounding biological variables that must be appreciated and should be controlled for when designing and interpreting efficacy studies. Having identified the most critical of these biological variables, we subsequently instituted parameters for optimal study design in the SOD1G93A mouse model. We retested several compounds reported in major animal studies (minocycline, creatine, celecoxib, sodium phenylbutyrate, ceftriaxone, WHI-P131, thalidomide, and riluzole) using this optimal study design and found no survival benefit in the SOD1G93A mouse for any compounds (including riluzole) administered by their previously reported routes and doses. The presence of these uncontrolled confounding variables in the screening system, and the failure of these several drugs to demonstrate efficacy in adequately designed and powered repeat studies, leads us to conclude that the majority of published effects are most likely measurements of noise in the distribution of survival means as opposed to actual drug effect. We recommend a minimum study design for this mouse model to best address and manage this inherent noise and to facilitate more significant and reproducible results among all laboratories employing the SOD1G93A mouse. Key words: G93A mice, riluzole, pre-clinical, SOD1, FALS Introduction Amyotrophic lateral sclerosis (ALS) is a paralytic neurodegenerative disorder caused by the loss of motor neurons. About 3% of cases are caused by single point mutations in the gene encoding SOD1. The identification of SOD1 as the mutated protein in a significant subset of FALS (1) has led to the generation of transgenic rodent models of autosomal dominant SOD1 FALS. The 23-copy human SOD1- G93A transgenic mouse (referred to hereafter as SOD1G93A) (2), a mixed hybrid strain, is the most widely used murine model of FALS and is accepted as a standard model for therapeutic studies since Gurney described its use (3). At least 50 publications describe therapeutic agents, from small molecules to viral vectors, that extend the lifespan of this SOD1G93A mouse (reviewed in (4,5); complete list of references in Table S1). Due to the rapid, unremitting disease course of ALS, these agents often quickly advance into clinical trials. However, to date, no therapy besides riluzole (with its modest effect of possibly two months life extension (6)) has demonstrated a significant impact on the course of the human disease (4,5). In the past five years we have screened more than 70 drugs in 18000 mice across 221 studies, using rigorous and appropriate statistical methodologies. We used the same strain of SOD1G93A mice used in