By The Numbers


Alzheimer’s disease has no cure. Yet.

 

Research is the only path to a cure.

Since 2004, Cure Alzheimer’s Fund has taken a unique approach to funding research with the highest probability of preventing, slowing or reversing Alzheimer’s disease.

 

Enabling the world’s leading scientists to explore bold ideas and make game-changing discoveries.

 

We can do this because of you.

 

Together we are making an impact.

All CureAlz figures above reflect inception in 2004 through Dec. 31, 2024.

Science Collaboration


Collaboration and information sharing are core principles of Cure Alzheimer’s Fund, fostering a cooperative environment among the researchers we support. By working together across subdisciplines and institutions, our funded scientists leverage each other’s discoveries and insights, accelerating progress in Alzheimer’s research. These research partnerships play a crucial role in deepening our understanding of the disease and leading to potential solutions.

 

Consortia Model

CureAlz supports new high-risk, high-potential standalone grants while also supporting larger-scale investigations within specific areas of the science. The consortia model empowers these initiatives with an expanded level of collaboration. To read additional detail about each consortium, please visit CureAlz.org/the-research/consortia/.

Alzheimer’s Disease Tau Consortium

Neurofibrillary tau tangles emerge and propagate in the Alzheimer’s brain at the same time that cognitive symptoms emerge. Tau’s role in Alzheimer’s disease (AD) and how it is induced by amyloid beta pathology are essential to understanding this disease. This consortium is investigating the initiation of tau pathology, neuron vulnerability and many other areas of AD tau biology.

Brain Entry and Exit Consortium

The brain is a remarkable but fragile organ that requires constant flows of nourishment in and debris out, but it has limited ability to renew itself if damaged by infection. A complex system of checkpoints controls the passage of materials between the brain and the rest of the body; the Brain Entry and Exit Consortium is investigating how these structures and the fluids that circulate among them function together to maintain health.

Fleming APOE Consortium

APOE4 is the strongest negative genetic risk factor for late-onset sporadic Alzheimer’s disease identified to date, whereas APOE2 is protective. Founded in 2017, this consortium is examining the many pathways in which the APOE protein plays a role to determine the mechanisms of its large impact on disease risk and progression.

Microbiome Consortium

The gut microbiome includes trillions of microorganisms, including bacteria, fungi and viruses, that live in the digestive tract and play an essential role in maintaining our health. Changes to composition of the gut microbiome can alter the state of our brains. This consortium is interrogating links between the gut microbiome and Alzheimer’s disease.

Neuroimmune Consortium

Our immune system, including the neuroimmune system of the brain, responds to both pathogens and everyday biological debris. The response must be proportionate and appropriate to the trigger, or else beneficial inflammation can turn damaging. The Neuroimmune Consortium is studying how the brain optimally recognizes and responds to AD pathology.

 

Advisory Groups

The collaborative efforts at Cure Alzheimer’s Fund include groups of researchers working together to guide research distributions. Two advisory groups made up of esteemed researchers share their expertise, participate in several meetings throughout the year, and work closely with our staff to facilitate collaboration and disseminate research findings to the broader community.

Research Leadership Group (RLG)

The RLG includes 41 leading scientists in the field of Alzheimer’s disease. These leaders are the primary decision makers regarding our overall direction, as well as for specific proposals and projects. The RLG recruits investigators, conducts peer reviews on research proposals and reports, participates in quarterly meetings and drives collaboration.

Randall J. Bateman, M.D.
Washington University School of Medicine in St. Louis

Mathew Blurton-Jones, Ph.D.
University of California, Irvine

Guojun Bu, Ph.D.
The Hong Kong University of Science and Technology

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

Marco Colonna, M.D.
Washington University School of Medicine in St. Louis

Laura M. Cox, Ph.D.*
Brigham and Women’s Hospital; Harvard Medical School

Bart De Strooper, M.D., Ph.D.
VIB-KU Leuven, Belgium; University College London, England

Marc I. Diamond, M.D.
University of Texas Southwestern Medical Center

P. Murali Doraiswamy, MBBS, FRCP
Duke University School of Medicine

Karen E. Duff, Ph.D.
University College London, England

Caleb E. Finch, Ph.D.
University of Southern California

Li Gan, Ph.D.
Weill Cornell Medicine

Samuel E. Gandy, M.D., Ph.D.
Icahn School of Medicine at Mount Sinai

Charles Glabe, Ph.D.
University of California, Irvine

Alison M. Goate, D.Phil.*
Icahn School of Medicine at Mount Sinai

Teresa Gomez-Isla, M.D.*
Massachusetts General Hospital; Harvard Medical School

Christian Haass, Ph.D.
German Center for Neurodegenerative Diseases (DZNE), Germany

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

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

Costantino Iadecola, M.D.*
Weill Cornell Medical College

Nancy Ip, Ph.D.
The Hong Kong University of Science and Technology

Jonathan Kipnis, Ph.D.
Washington University School of Medicine in St. Louis

Bruce Lamb, Ph.D.
Indiana University School of Medicine

Christoph Lange, Ph.D.
Harvard T.H. Chan School of Public Health

Cynthia A. Lemere, Ph.D.
Brigham and Women’s Hospital; Harvard Medical School

Yueming Li, Ph.D.
Memorial Sloan Kettering Cancer Center

Shane A. Liddelow, Ph.D.
New York University

William C. Mobley, M.D., Ph.D.
University of California, San Diego

Ronald C. Petersen, M.D., Ph.D.
Mayo Clinic, Rochester

Leonard Petrucelli, Ph.D.*
Mayo Clinic, Jacksonville

Sangram S. Sisodia, Ph.D.
The University of Chicago

Beth Stevens, Ph.D.
Boston Children’s Hospital; Harvard Medical School; Broad Institute

Li-Huei Tsai, Ph.D.
Massachusetts Institute of Technology; Broad Institute

Robert Vassar, Ph.D.
Northwestern University Feinberg School of Medicine

Cheryl Wellington, Ph.D.
University of British Columbia, Canada

Stephen T.C. Wong, Ph.D.
Houston Methodist Research Institute; Weill Cornell Medicine

Tony Wyss-Coray, Ph.D.
Stanford University

Riqiang Yan, Ph.D.
University of Connecticut Health Center

Andrew S. Yoo, Ph.D.*
Washington University School of Medicine in St. Louis

Hui Zheng, Ph.D.
Baylor College of Medicine

Rudolph E. Tanzi, Ph.D. Chair
Massachusetts General Hospital; Harvard Medical School

*New member

 

Scientific Advisory Board (SAB)

The role of the SAB is to provide guidance to Cure Alzheimer’s Fund regarding its overall scientific direction and funding efficacy. The members—who have broad experience bringing therapeutics to patients—review the entire research portfolio to ensure that CureAlz is supporting investigations into the most important issues in Alzheimer’s disease, and that our funding mechanisms accelerate the path to patients.

Vince Groppi, Ph.D.
Oricula Therapeutics

John S. Lazo, Ph.D.
University of Virginia

Patrick C. May, Ph.D.
Advantage Neuroscience Consulting LLC

Karen Reeves, M.D.
Ligand Pharmaceuticals

Steven M. Paul, M.D. Chair
Seaport Therapeutics

Looking Forward


Cure Alzheimer’s Fund entered 2025 with a strong portfolio of compelling scientific ideas and, as the year has progressed, that portfolio has only grown. Our Research Leadership Group—made up of leading scientists in the field—continues to guide us in making strategic funding decisions and identifying high-priority areas for investigation. The study of aging across its many aspects is a priority for 2025.

 

Alzheimer’s disease does not happen without aging. While the connection between aging and Alzheimer’s has long been clear, aging itself is poorly understood and not well-defined. Not everyone ages the same way, at the same rate, or experiences the same kind of cognitive decline. Each of our cells, organs and systems ages individually as well as together; new discoveries and technologies allow us to investigate the changes that come with age in astonishing new ways. Understanding what drives healthy aging is critical to identifying what is normal and what may be a function of disease.

Many biological changes linked to aging influence brain health. For instance, chronic, low-grade inflammation in the body is a common feature of aging. Scientists now know that the body’s immune system interacts with the brain, and chronic inflammation increases disease risk. Exploring ways to reduce overall inflammation in the body can create a healthier brain environment to support cognitive resilience.

Another sign of aging is dysregulated proteostasis, which encompasses all the processes that regulate how proteins are produced, folded and cleared within a cell. Because proteins are involved in virtually every process in the body, ensuring their proper regulation is critical for overall health. Proteostasis declines with age and is linked to age-related disorders like Alzheimer’s, where misfolded amyloid and tau proteins accumulate in the brain and cannot be effectively cleared away. Understanding how age disrupts proteostasis—and uncovering ways to restore it—could extend healthy aging and reduce disease pathology.

In addition to biological factors, aging is shaped by the exposome—the cumulative impact of environmental and lifestyle factors over a lifetime. While we can’t change genetic factors, as individuals and as societies, we can influence modifiable factors such as education access and diet quality. Research into the exposome will help identify ways to reduce Alzheimer’s risk and promote brain health.

Defining healthy aging is only one part of understanding how to promote brain health. Another approach is the study of super-agers—individuals who remain cognitively vibrant well into their ninth and even 10th decades. These remarkable individuals often possess genetic traits that protect against dementia, offering valuable insights into how the brain can stay healthy for a lifetime. By studying super-agers, researchers hope to design interventions that help more people achieve cognitive longevity.

At Cure Alzheimer’s Fund, we are committed to unlocking the secrets to lifelong brain health and identifying early disease markers. By understanding how to protect the brain as we age, we move closer
to preventing Alzheimer’s before it starts.

The groundbreaking research we support is drawing us nearer to an end to Alzheimer’s disease. Your generosity fuels this progress, and for this, we are truly grateful.