Dr. Fen-Biao.Gao, Dr. Sandra C. Almeida, Angel Fund President Rich Kennedy,Dr. Claudia Fallini,

Dr. Fen-Biao.Gao, Dr. Sandra C. Almeida, Angel Fund President Rich Kennedy,Dr. Claudia Fallini,

You have supported a researcher!

Great news! the researchers have been “adpoted”. Thanks to the Phi Gamma Delta fraternity’s ice bucket challenge, the two researchers have new supporters!

The ice bucket challenge was held in memory of Steve Rubin, a fraternity brother who lost his courageous battle with ALS.

The researchers at the Day Lab at UMass Medical School work tirelessly to find a cure for ALS. Each lab has remarkable researchers who work on individual pieces of the puzzle that fit into the whole research picture.

The Angel Fund for ALS Research would like to introduce you to two remarkable researchers who are new Angel Fund Fellows: Dr. Sandra Almeida and Dr. Claudia Fallini. We invite you to “adopt” one of these Fellows. The adoption process is simple: to adopt a Fellow, the Angel Fund supporter will contribute towards a total of $25,000 to support the research of these individuals.

Regardless of whether you are a business, a family or an individual, by adopting a research Fellow you can help Dr. Brown and the UMass ALS research team reach their goal – finding a treatment and a cure for ALS.

If you adopt the Angel Fund Fellow, you will be invited to come the Day Lab at UMass Medical School to meet the researchers and gain an inside view of their cutting edge research.As a donor, you will also get research updates from their lab.

 Donate Now




Researcher Assistant Professor
with Dr. Fen-Biao Gao

Dr. Almeida writes: “I was born in a very small village in Portugal, but grew up in Coimbra, a city of approximately 100,000 people. I liked school from an early age, and always tried to do my best. My parents were very proud when I was accepted to attend the University of Coimbra. During college, I swam regularly at a large indoor pool in the city, and began taking evening classes to improve my English.

I went on to do my doctoral training at the University of Coimbra, and during this time I was able to travel to several international conferences. My first time visiting the US was at a Society for Neuroscience meeting in New Orleans. A few years after that, I was accepted to do an 8-month study abroad funded by the Portuguese Foundation, in which I worked as a visiting scientist at the Buck Institute for Research on Aging.

Upon completing my Ph.D., I joined the laboratory of Dr. Fen-Biao Gao, the leading stem cell scientist in ALS -frontotemporal dementia (ALS-FTD), at the Gladstone Institute of Neurological Disease in San Francisco and initiated the induced pluripotent stem (iPS) cell work in his laboratory. Six years ago, I moved with Dr. Gao’s group to UMass Medical School in Worcester, where I am currently a Research Assistant Professor and continue to study ALS/FTD such as those with C9ORF72 repeat expansions. I really hope to find a cure for these diseases as soon as possible.

Lastly, and most importantly, my husband and I have a beautiful 18-month old daughter, Emilia, who is sweet, adorable, and surprises us daily with her cleverness.

Dr. Almeida’ s Research

We generate induced pluripotent stem cells (iPSCs) from skin fibroblast cells of ALS/FTD patients with C9ORF72 repeat expansions and other genetic mutations. We differentiate these iPSCs into human motor neurons and cortical neurons to study disease mechanisms and identify potential therapeutic targets.  Some of these studies have been published in leading journals such as Nature, Nature Medicine and Neuron. Currently, we are very excited about a few suppressor genes whose partial loss of function can decrease toxic products of C9ORF72 repeat expansions. We hope after further investigation, these suppressor genes can serve as molecular targets for therapeutic interventions in ALS/FTD patients with C9ORF72 repeat expansion.”



Research Assistant Professor with 
Dr. John Landers 

Three years ago, Dr. Landers and Brown identified an important ALS gene in a large family from Israel and France. The discovery of this gene, called profilin-1, led not only to improved understanding of some types of ALS but also to a new mouse model of ALS. In fact, this is the most important mouse model in ALS since the first SOD1 model in 1994. Dr. Fallini has been an important member of the Landers team working closely on profiling-1 since it was discovered.

Dr. Fallini has received her Ph.D. from the Università degli Studi di Milano (Italy) in 2009, where she gained interest in the basic cellular and molecular mechanisms leading to neurodegeneration. In particular, she focused her studies on the role of mRNA regulation in the maintenance and function of motor neurons.

After she graduated, she moved to the US to start her postdoctoral training in the laboratory of Dr. Gary Bassell at Emory University (Atlanta, GA). There, she continued to pursue her research interests in neurodegeneration and applied her skills to the study of the motor neuron diseases SMA and ALS. This led to five first-author publications and several co-authorships, including the discovery of mutations in the profilin-1 gene as causative for ALS, in collaboration with Dr. John Landers, a former Angel Fund Fellow, at UMASS (Worcester, MA).

Claudia is a passionate reader and music lover. Being Italian, she loves classical music and opera and, of course, great food. But her true passions are her lovely husband Francesco and adorable 2-year-old daughter Emma.

Dr. Fallini’s Research

Dr. Fallini moved to Dr. Landers’ lab in 2012 to continue her research on the study of the molecular mechanisms leading to ALS. This effort led to a co-first authorship on the discovery of another ALS gene called α-tubulin isoform 4A. Drs. Fallini and Landers discovered that mutations in the α-tubulin isoform 4A gene are associated with familial ALS (published in the journal Neuron, 2014).

Dr. Fallini was promoted to the rank of Research Assistant Professor in September 2015. She is focusing her studies of investigation of the molecular mechanisms and functional consequences of cytoskeletal alterations on the maintenance of motor neurons by using cellular and animal models of ALS.