The Sturge-Weber Foundation’s (SWF) international mission is to improve the quality of life for people with Sturge-Weber syndrome through collaborative education, advocacy, and research support.
Current Grant Application Openings:
New Horizon Research Grant
SWF invites all qualified clinicians or scientists at universities, hospitals, and research institutions (not-for-profit or for-profit) to submit applications for the New Horizon Research Grant. This grant application is open to medical schools, residents, or postdoctoral faculty who support research relevant to our mission.
The goal of this Grant is to support patient-oriented research or surveys, basic science research, or translational studies relevant to Sturge-Weber syndrome (SWS) or related conditions, and to increase SWS publications.
Possible areas of research include, but are not limited to:
- Epidemiological
- Behavioral Studies
- Small Clinical Exploratory Trials
- Studies in Quality of Life Devices
- Programs focusing on the Neurological, Ophthalmological, and Dermatological manifestations of SWS
Award Grant: $5,000-10,000
Information Required From the Candidate:
Please provide this in a single PDF file.
- Current biosketch in NIH format from both the applicant and list his/her mentor.
- A four-page proposal including the following information (including any figures or tables):
- Title
- Specific Aims
- How will this award advance the missions of the SWF statement above
- Background and significance
- Research strategy
- A brief summary of the training plan from the applicant’s perspective
Questions? Contact the Foundation at swf@sturge-weber.com
To participate, fill out the form below.
Seed Grant
The Sturge-Weber Foundation’s (SWF) international mission is to improve the quality of life for people with Sturge-Weber syndrome through collaborative education, advocacy, and research support. SWF invites all qualified scientists at universities, hospitals, and research institutions (not-for-profit or profit) to submit applications for the Seed Grant, a postdoctoral fellowship that supports research relevant to our mission.
The goal of this Grant is to support patient-oriented research, basic science research, or translational studies relevant to Sturge-Weber syndrome or related conditions. Possible areas of research include, but are not limited to, epidemiological, or behavioral studies, small clinical exploratory trials, studies of disease mechanisms, and the development of new technologies, biomarkers, and treatments focusing on the
neurological, ophthalmological, and dermatological manifestations of SWS.
Award Grant: Up to $5000 per project
Information Required From the Candidate:
- Current biosketch in NIH format from both the applicant and list his/her mentor.
- A four-page proposal including the following information (including any figures or tables):
- Title
- Specific Aims
- How will this award advance the missions of the SWF statement above
- Background and significance
- Research strategy
- A brief summary of the training plan from the applicant’s perspective
Questions? Contact the Foundation at swf@sturge-weber.com
To participate, fill out the form below.
Catalyst Research Grant
The Sturge-Weber Foundation’s (SWF) international mission is to improve the quality of life for people with Sturge-Weber syndrome through collaborative education, advocacy, and research support. SWF invites all qualified scientists at universities, hospitals, and research institutions (not-for-profit or profit) to submit applications for the Catalyst Research Grant, a postdoctoral fellowship that supports research relevant to our mission.
The goal of this Grant is to support patient-oriented research, basic science research, or translational studies relevant to Sturge-Weber syndrome or related conditions. Possible areas of research include, but are not limited to, epidemiological, or behavioral studies, small clinical exploratory trials, studies of disease mechanisms, and the development of new technologies, biomarkers, and treatments focusing on the
neurological, ophthalmological, and dermatological manifestations of SWS.
Award Grant: $30,000 - $50,000
Information Required From the Candidate:
- Current biosketch in NIH format from both the applicant and list his/her mentor.
- A four-page proposal including the following information (including any figures or tables):
- Title
- Specific Aims
- How will this award advance the missions of the SWF statement above
- Background and significance
- Research strategy
- A brief summary of the training plan from the applicant’s perspective
Questions? Contact the Foundation at swf@sturge-weber.com
To participate, fill out the form below.
2025-2026 Research Grant Awards
Sturge-Weber Foundation Catalyst Research Grants:
Investigator: Sana Nasim, Ph.D.
Title: Development of GNA11 p.R183C endothelial-specific in vitro model
Award Amount: $7,800
Specific Aims: Our goal is to develop an in vitro GNA11 p.R183C model to investigate the underlying disease mechanisms. To achieve this, we will employ CRISPR/Cas9 genome editing to introduce the GNA11 R183C mutation in human endothelial cells (ECs).
How this award will advance the missions of the SWF: The proposed work aligns with the mission of the Sturge-Weber Foundation, which supports research aimed at uncovering the mechanisms driving capillary malformations, identifying mutation-specific drug targets, and developing innovative in vitro technologies. I
Investigator: Joyce Bischoff
Affiliation: Boston Children’s Hospital and Harvard Medical School
Investigators: Sana Nasim, Ph.D. and Joyce Bischoff, Ph.D.
Title: GNAQ p.R183Q impact on PI3K/AKT signaling opens new possibilities for drug targeting
Award Amount: $6,357
Specific Aim: To measure PIP2 levels in GNAQ mutant versus wild-type endothelial cells to determine if the constitutive activation of Gαq reduces PIP2 substrate available for PI3Kα, an enzyme that initiates a fundamental pathway in vascular homeostasis (Figure 1).
How this award will advance the mission of the SWF We propose pharmacologic activation of the PI3Kα pathway will reduce the elevated angiopoietin-2 (ANG2, aka ANGPT2) and restore a normal endothelial barrier to blood vessels with GNAQ p.R183Q endothelial cells. This novel concept is supported by preliminary data from our lab and presents an opportunity to test new strategies for reversing the deleterious impacts of the constitutive Gαq signaling in SWS.
Investigator: Padmanabhan Pattabiraman, PhD
Affiliation: Indiana University Assistant Professor
Eugene and Marilyn Glick Eye Institute, Department of Ophthalmology
Title: Clusterin-based therapy for ocular hypertension and glaucoma treatment in Sturge-Weber Syndrome
Award Amount: $15,000
Background and Scientific Premise: Towards understanding the role of clusterin in the regulation of intraocular pressure (IOP), my lab has identified that loss of clusterin function increased IOP and induction of clusterin production or supplementation of recombinant clusterin lowers IOP. These systematic data pointed us to understand the mechanistic evidence towards IOP lowering. Our unbiased proteomics studies revealed that Clusterin acted as a signal attenuator by lowering lowered profibrotic SMAD3 that is a primary downstream signaling molecule involved in canonical TGFb signaling, G-proteins including GNAQ, GNB1, and GNG12; and Ras-related RRAS2. In our continuing research, we show that inactivating GNAQ lowers the IOP by decreasing actin-based contractility and ECM remodeling in trabecular meshwork. GNAQ gene codes for the alpha subunits of the heterotrimeric G proteins, Gαq. Gαq can act as a molecular switch relaying signals from outside the cell to the inside, influencing gene expression, cell growth, and tissue morphogenesis. Interestingly, a constitutive active variant of GNAQ, p.R183Q, results in early-onset hypertension and secondary glaucoma in patients with Sturge-Weber syndrome (SWS) secondary glaucoma. We are interested in targeting mutant GNAQ using Clusterin in the trabecular meshwork outflow pathway.
Questions to be addressed: a) Does clusterin lower the effects of mutant Gnaq on IOP elevation and glaucomatous phenotype? b) What is the mechanistic evidence for clusterin in lowering Gnaq?
Strategy: AIM 1: To provide the proof of concept that mutant GNAQ can elevate IOP: Currently, we are preparing adenovirus overexpressing the wildtype and GNAQR183Q from plasmids obtained through Dr. Doug Marchuk. We plan to express the adenovirus wildtype and GNAQR183Q in: 1) the anterior segment perfusion cultures of human eyes ex vivo, and 2) mouse eyes via intravitreal injections in vivo to measure the IOP and see if constitutive active GNAQ can elevate IOP. Histological examination will be performed to confirm the structure-function correlate.
AIM 2: To test if clusterin can lower IOP elevation due to mutant GNAQ: In our ex vivo and in vivo model systems of IOP elevation due to GNAQR183Q, we will by supplementing clusterin into the anterior segment by providing recombinant clusterin or adeno/lentivirus expressing clusterin.
