While Cure Alzheimer’s Fund historically has supported smaller-scale research projects—one or two researchers working together and grants at the $100,000 to $300,000 level—advances in the understanding of Alzheimer’s warrant more significant research investigations within a specific area of the science. The Consortia model provides for an additional level of collaboration, and is therefore a fundamental part of Cure Alzheimer’s Fund’s approach to research funding.

Here are summaries of four of the Consortia currently in operation with grants from Cure Alzheimer’s Fund.


Three Dimensional Drug Screening Consortium


In 2014, Drs. Rudy Tanzi and Doo Yeon Kim resolved one of the critical challenges of Alzheimer’s disease research: how to grow human brain cells that exhibit the hallmarks of Alzheimer’s pathology in a form mimicking that of a live brain, i.e. a gel. This new tool allowed for a more thorough testing of existing drugs, to determine whether they should be considered for clinical trials.

In 2018, Drs. Tanzi and Hansang Cho expanded on the original system to culture neural stem cells that, in addition to having elevated levels of amyloid beta and tau, also have the inflammatory factors known to contribute to neuroinflammation in Alzheimer’s disease.

This human three-dimensional culture model (commonly known as ‘Alzheimer’s in a Dish’) has enormous potential to innovate and accelerate the Alzheimer’s drug screening process by providing large-scale, high-throughput screening for novel therapeutic targets. One major objective of the 3DDS consortia is to screen drugs that already have FDA-approval—thus repurposing drugs that have been screened for bioavailability and safety in human applications.

Scientists and Institutions:

Hansang Cho | Ph.D.
University of North Carolina at Charlotte

Se Hoon Choi | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Ana Griciuc | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Roger Kamm | Ph.D.
Massachusetts Institute of Technology

Doo Yeon Kim | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Joseph Park | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Rudy Tanzi | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Stephen Wong | Ph.D.
Houston Methodist Hospital; Weill Cornell Medical College

Weiming Xia | Ph.D.
Boston University School of Medicine



ApoE Consortium


ApoE (apolipoprotein e) is a class of proteins involved in the metabolism of fats in the body. The ApoE gene provides instructions for this class of proteins, and in 1993 a variant of ApoE gene—the e4 variant—was identified as a strong genetic risk factor for late-onset Alzheimer’s disease. Someone who inherits the ApoE4 gene from one parent is about 3.8 times more likely to develop Alzheimer’s disease. Inheriting 2 copies of ApoE4 increases risk approximately 12-fold.

In recent years, evidence has accumulated demonstrating that ApoE influences amyloid-beta deposition in the brain, suggesting a possible mechanism of action. Research suggests that while amyloid-beta is a key initiator of Alzheimer’s pathology, accumulation of tau in the brain strongly correlates with neurodegeneration. The link between ApoE and tau has not been fully explored. This consortium intends to collaborate in order to determine if ApoE can enhance tau-mediated neurodegeneration through a mechanism involving astrocytes and microglia-mediated pathways.

Scientists and Institutions:

Randy Bateman | Ph.D.
Washington University in St. Louis School of Medicine

Guojon Bu | Ph.D.
Mayo Clinic Jacksonville

Oleg Butovsky | Ph.D.
Brigham and Women’s Hospital; Harvard Medical School

Paul Greengard | Ph.D., Nobel Laureate
The Rockefeller University

David Holtzman | M.D.
Washington University in St. Louis School of Medicine

Cheryl Wellington | Ph.D.
University of British Columbia



Consortium to Infer Regulatory Circuits and to Uncover Innovative Therapeutic Strategies


The last decade of research into Alzheimer’s has uncovered more than 20 different genetic regions associated with the disease, including several genes involved in amyloid beta and tau protein accumulation. Recent genetic studies have provided hope in the search for a cure for our rapidly aging population, but translating genetic research into clinical trials has been a great challenge, in large part due to the fact that most genetic mutations affect the expression of nearby genes in subtle ways that are difficult to detect.

The Consortium to Infer Regulatory Circuits and to Uncover Innovative Therapeutic Strategies (CIRCUITS) brings together leading experts in Alzheimer’s disease and computational biology to use state-of-the-art technology to leverage large-scale genetic and genomic information for therapeutic target discovery.

The CIRCUITS Consortium will use its computational expertise to uncover the differences between the brains of those who were afflicted with Alzheimer’s disease and those who were not, including identification of regulatory regions that may be implicated in causing Alzheimer’s disease. This group seeks to create a vast repository of epigenetic information; the insights gleaned from the research will be made available to the broader scientific community to accelerate the study of Alzheimer’s disease.

Scientists and Institutions:

Lars Bertram | M.D.
University of Lubeck: Imperial College of London, UK

Joseph Ecker | Ph.D.
Salk Institute for Biological Studies

Winston Hide M.A. | Ph.D.
Beth Israel Deaconess Medical Center

Bradley Hyman | M.D., Ph.D.
Massachusetts General Hospital; Harvard Medical School

Rudolf Jaenisch | M.D.
Massachusetts Institute of Technology

Manolis Kellis | Ph.D.
Massachusetts Institute of Technology

Andreas Pfenning | Ph.D.
Carnegie Mellon University

Rudy Tanzi | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Li-Huei Tsai | Ph.D.
Massachusetts Institute of Technology



Gifford Neuroinflammation Consortium


More than half of the genes associated with risk for Alzheimer’s disease are selectively expressed in microglia, the first line of active immune defense in the central nervous system. Microglia respond dynamically to changes in the brain due to injury, infection, or other abnormalities. In this role, these cells can be both beneficial—removing toxic proteins and cellular debris—and detrimental—promoting neuroinflammation that leads to damaging synapse loss and interfering with normal cell signaling.

Very little is known about the underlying biology of microglia and how they contribute to Alzheimer’s disease.
This consortium brings together an interdisciplinary team of scientists to develop new approaches to understanding how microglia mediate helpful or harmful roles in the brain. In addition, the team is examining the complex and diverse function of microglia and astrocytes in order to characterize the changes that occur over the progression of the disease. These scientists are actively building a comprehensive map of immune and neural cell state changes that occur in Alzheimer’s disease and normal aging.

Scientists and Institutions:

Sandeep Robert Datta | M.D., Ph.D.
Harvard Medical School

Christopher K. Glass | M.D., Ph.D.
University of California, San Diego School of Medicine

Jacob Hooker | Ph.D.
Massachusetts General Hospital; Harvard Medical School

Shane Liddelow | Ph.D.
New York University School of Medicine

Beth Stevens | Ph.D.
Boston Children’s Hospital; Harvard Medical School

Cure Alzheimer’s Fund is a non-profit dedicated to funding research with the highest probability of preventing, slowing, or reversing Alzheimer’s disease. Our Board pays for all overhead expenses: 100% of your donation will go to research.