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, 2023.


Since our founding, CureAlz has mandated—and our affiliated researchers have appreciated—that open discussion and collaboration are vital to participation in our community. Through cooperative efforts, researchers benefit from the findings and input of others, accelerating the growth of knowledge. Our funded researchers actively engage across subdisciplines and institutions to build research partnerships and together contribute significantly to a better understanding of Alzheimer’s disease (AD).


Consortia Model

Cure Alzheimer’s Fund historically has supported innovative research projects, with grants at the $100,000 to $300,000 level, that have the potential to add significant new understanding of Alzheimer’s pathology to the field. While CureAlz continues to enthusiastically support these standalone high-risk, high-potential efforts, advances in understanding Alzheimer’s disease have warranted larger-scale investigations within specific areas of the science. The consortia model provides for organized, large-scale initiatives with an expanded level of collaboration and shared cross-institutional goals.

In 2023, 24% of research spending went toward five active consortia. Each consortium had a regular schedule of meetings throughout the year that brought lab leaders and personnel together to discuss progress, share findings, offer encouragement and ensure productive collaborations. After several grant cycles, this year we closed the Alzheimer’s Disease Drug Discovery and Development (AD4) and the Collaboration to Infer Regulatory Circuits and Uncover Innovative Therapeutic Strategies (CIRCUITS) consortia and transitioned some of the projects to standalone awards. We launched a “refreshed” Neuroimmune Consortium and a new Microbiome Consortium.

Alzheimer’s Disease Tau Consortium

A considerable amount is known about the involvement of tau in neurodegenerative diseases where it is the main contributing pathology, known as primary tauopathies. However, tau’s role in Alzheimer’s disease, a secondary tauopathy in which tau pathology develops in an AD-specific pattern in response to amyloid beta, is less clear. Given that tau is so closely associated with neurodegeneration and cognitive impairment in AD, a deeper understanding is necessary to enable improved diagnostic and prognostic biomarkers, as well as to identify new opportunities for effective therapeutic intervention. The Alzheimer’s Disease Tau Consortium brings together leaders with the expertise and motivation to shed light on tau’s complex role specifically in Alzheimer’s disease.

FLEMING APOE (Apolipoprotein E) Consortium

Substantial data inform us that APOE gene variants differentially affect risk for developing sporadic Alzheimer’s disease, yet the mechanisms that explain this are not understood. Increased risk may arise from how APOE affects amyloid plaque accumulation and clearance, tau tangle formation, neuroinflammation, non-Alzheimer’s disease hallmarks of aging and the porosity of the blood-brain barrier. The Fleming APOE Consortium brings together experts to develop a better understanding of these mechanisms.

Brain Entry and Exit Consortium

The brain is a remarkable but fragile organ with limited ability for self-renewal following injury; it also has a very high metabolism, using approximately 20% of all energy consumed by the body and producing significant waste. Consequently, it has evolved a complex system of barriers to control the entry and exit of materials and maintain its delicate healthy balance. The Brain Entry and Exit Consortium is investigating how each component of the brain’s entry and exit structures, along with the cerebrospinal fluid that flows through the brain, must function together to maintain health.

Microbiome Consortium

The gut microbiome is the community of trillions of microorganisms, including bacteria, fungi and viruses, that live in the digestive tract. These microbes play an essential role in maintaining our health, and emerging research suggests there may be a link between the gut microbiome and Alzheimer’s disease. The Microbiome Consortium represents a group of world-renowned Alzheimer’s disease (AD) researchers who will take a multifaceted approach to investigating the mechanisms by which the microbiome impacts Alzheimer’s disease. Work by the consortium also includes uncovering the full spectrum of microbes that may be present in the AD brain to understand the potential role of infections driving AD pathology.

Neuroimmune Consortium

Neuroinflammation is a well-known feature of Alzheimer’s disease dating back to the description of reactive glial cells in the brain by Alois Alzheimer more than 100 years ago. Modern research shows that this inflammatory response is not just an innocent bystander during disease progression. Many genetic risk factors for sporadic Alzheimer’s disease affect the brain’s immune cells—microglia and astrocytes. The researchers in the Neuroimmune Consortium are mapping out the roles of these and other immune cells in the brain during Alzheimer’s disease.

“Cure Alzheimer’s Fund has enabled us to take big risks on new ideas, speeding movement into new and novel spaces for research and accelerating science out of the lab and (ultimately) into the clinic. Even more important is the expansive network of Alzheimer’s disease experts that are always on hand to provide insights, advice and support to push these discoveries ever further forward.”



Advisory Groups and Meetings

The collaborative efforts at Cure Alzheimer’s Fund also include groups of researchers working together to help set priorities and drive the direction of research distributions. Two advisory groups, made up of esteemed researchers, share their expertise and participate in several meetings throughout the year to facilitate collaboration and disseminate research findings to the broader community.

Research Leadership Group (RLG)

The 2023 RLG included 39 leading scientists specializing in Alzheimer’s disease and related fields. These leaders are the primary decision makers regarding our overall direction, as well as whether to support specific proposals and projects. The RLG refers investigators, conducts peer reviews on research proposals and reports, participates in quarterly meetings and drives collaboration.

Scientific Advisory Board (SAB)

The role of the SAB is to provide guidance to Cure Alzheimer’s Fund regarding our overall scientific direction and funding impact. 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 benefits for patients.

International Conference Attendance and Sponsorship

Cure Alzheimer’s Fund was a sponsor of the International Conference on Alzheimer’s Disease and Parkinson’s Diseases (AD/PD) held in March 2023 in Gothenburg, Sweden. This annual conference is the largest global conference dedicated to basic science and translational and clinical research, and featured many of our funded researchers and projects.

“Cure Alzheimer’s Fund support sparked a collaboration between two investigators who on the surface appear to study two totally different topics. Together we teamed up to think about Alzheimer’s disease from a new perspective.”



Published Papers

Once a researcher has completed their work, they document the details and outcomes of their study and submit the paper for publication in a science journal. The paper is peer reviewed by scientists to validate the methods and information and, if approved, gets published so the results can be shared with the world. Cure Alzheimer’s Fund tracks published papers as one key measure of success for research grants that we funded.

In 2023, 183 peer-reviewed papers that acknowledged support from Cure Alzheimer’s Fund were published in prominent scientific journals, more than in any year before. Since our inception in 2004 through Dec. 31, 2023, the total number of published papers acknowledging CureAlz funding is 1,177. These published papers collectively have been cited by other researchers in support of their own work 97,674 times.

Here are a few select highlights from papers published resulting from CureAlz-funded research in 2023.

Unlocking the Brain’s Immune Gateways—The Role of Skull Channels in Neuroimmune Communication

The central nervous system (CNS), made up of the brain and spinal cord, has a specialized immune system that historically has been considered isolated from the immune system that serves the rest of the body. However, recent research has challenged this idea by demonstrating an intricate relationship between the two systems. Newly discovered skull channels connect bone marrow within the skull with the protective layers surrounding the brain, suggesting that the bone marrow contributes white blood cells to guard the CNS. Read more here.

Published in Nature Neuroscience: “Skull bone marrow channels as immune gateways to the central nervous system”

Jonathan Kipnis, Ph.D., Washington University School of Medicine in St. Louis, and Matthias Nahrendorf, M.D., Ph.D., Massachusetts General Hospital; Harvard Medical School

Exercise and Alzheimer’s Disease: The Protective Power of Irisin*

Using a 3D cell culture model that generates Alzheimer’s disease pathology, scientists discovered that the hormone irisin, which is released from the muscles during exercise, increases the production of neprilysin in specific brain cells known as astrocytes. Upon its release from astrocytes, neprilysin breaks down amyloid beta, the protein that forms harmful plaques in AD. In these experiments, exposure to the exercise-triggered hormone irisin led to significant reduction in amyloid beta levels. Read more here.

Published in Neuron: “Irisin Reduces Amyloid-ß by Inducing the Release of Neprilysin from Astrocytes Following Downregulation of ERK-STAT3 Signaling”

Joseph Park, Ph.D., Luisa Quinti, Ph.D., Doo Yeon Kim, Ph.D., Christiane Wrann, D.V.M, Ph.D., Rudolph Tanzi, Ph.D., and Se Hoon Choi, Ph.D., Massachusetts General Hospital; Harvard Medical School

*Research has highlighted the benefits of exercise for brain health, including for Alzheimer’s disease. The discovery of the hormone irisin and its interaction with amyloid plaques is one mechanism for exercise’s positive impact.

The Brain’s Blood Vessels Change in Alzheimer’s Disease

Changes in the blood vessels of the brain have been linked to Alzheimer’s disease (AD), and deterioration of the blood-brain barrier may be an early sign of the disease. A study profiling gene expression of the brain’s blood vessels revealed AD changes in unprecedented detail. The results provide a map to guide future therapies targeting blood-brain barrier dysfunction in Alzheimer’s. Read more here.

Published in Nature Neuroscience: “Single-nucleus multiregion transcriptomic analysis of brain vasculature in Alzheimer’s disease”

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

Role of T Cells in Alzheimer’s Disease Identified

With age and cell damage, microglia can shift from protective to destructive.

A new study reveals that mice with loss of brain tissue caused by toxic tau, similar to that in Alzheimer’s, have more destructive T cells, generally resident in the periphery of the body, in their brains, attracted there by the brain-resident microglia. Understanding the role of these circulating immune cells in neurodegeneration may lead to new areas of therapeutic strategies. Read more here.

Published in Nature: “Microglia-Mediated T Cell Infiltration Drives Neurodegeneration in Tauopathy”

Jasmin Herz, Ph.D., Jonathan Kipnis, Ph.D., Jason D. Ulrich, Ph.D., and David M. Holtzman, M.D., Washington University School of Medicine in St. Louis

“CureAlz funds accelerated discovery in the type of research we do, speeding up to find answers to the questions we are asking.”


Why Are Some People Resilient to Alzheimer’s Disease Pathology?

Despite high levels of amyloid beta plaques and tau tangles in their brain, some individuals never develop symptoms of dementia in their lifetime. Resilience to pathology leading to Alzheimer’s disease may be associated with reduced levels of neuroinflammation, preserving synapses and staving off neurodegeneration. This study suggests that in cases with symptoms of Alzheimer’s disease, neuroinflammation may be triggered by an unusual abundance of toxic tau oligomers in synapses that serve as an “eat me” signal to microglia and astrocytes. In contrast, resilient brains show lower levels of tau oligomers and preserved synapse numbers. Read more here.

Published in JAMA Neurology: “Tau Oligomer-Containing Synapse Elimination by Microglia and Astrocytes in Alzheimer Disease”

Teresa Gomez-Isla, M.D., Massachusetts General Hospital; Harvard Medical School, and Karen E. Duff, Ph.D., University College London, England

Insights from the Aging Mouse Brain

This investigation set out to identify the molecular underpinnings of aging in the brain. It discovered that previously unsuspected regions of the brain are especially vulnerable to aging, and that two anti-aging treatments can rejuvenate the brain in unexpected ways. Read more here.

Published in Cell: “Atlas of the Aging Mouse Brain Reveals White Matter as Vulnerable Foci”

Tony Wyss-Coray, Ph.D., Stanford University

Does a Genetic Mutation Prevent Alzheimer’s Disease?

In a study exploring the interaction between genetics and Alzheimer’s disease pathology, researchers discovered how the APOE3 Christchurch (APOE3ch) mutation protects against Alzheimer’s disease. The findings showcase how APOE3ch revs up the efficiency of microglia surrounding amyloid plaques to remove aggregated tau and has the ability to prevent the spread of tau, which precedes neuronal death and dementia. Read more here.

Published in Cell: “APOE3ch Alters Microglial Response and Suppresses Aß-Induced Tau Seeding and Spread”

Marco Colonna, M.D., Jason D. Ulrich, Ph.D., and David M. Holtzman, M.D., Washington University School of Medicine in St. Louis

The First Biomarker for Tau Tangles

Researchers have identified a promising biomarker, MTBR-tau243, that could transform the early detection of Alzheimer’s disease. The strong association of MTBR-tau243 with tau pathology and cognitive decline positions it as a prime candidate for diagnosing Alzheimer’s disease, tracking its advancement and evaluating tau-targeted therapies.

Published in Nature Medicine: “CSF MTBR-tau243 is a specific biomarker of tau tangle pathology in Alzheimer’s disease”

David M. Holtzman, M.D., and John C. Morris, M.D., Washington University School of Medicine in St. Louis; Rik Ossenkoppele, Ph.D., Amsterdam University Medical Center, The Netherlands; Lund University, Sweden; Oskar Hansson, M.D., Ph.D., Lund University, Sweden; Randall J. Bateman, M.D., Washington University School of Medicine in St. Louis

“Funding from Cure Alzheimer’s Fund helped my lab make some important discoveries that have now launched a major area of research for us and led to several NIH grants, as well as a new drug discovery effort. So, the impact has been huge.”


Follow on Funding

Our grants for proof-of-concept, early-stage research provide the resources to generate
necessary data, leading to follow-on funding from the National Institutes of Health
(NIH)/National Institute on Aging (NIA).


“Support from Cure Alzheimer’s Fund has allowed us to take risks and initiate projects quickly, without waiting years for NIH funding. It has also allowed us to build up preliminary data that has enabled us to get longer-term funding from the NIH.”



Looking Forward

This year, our 20th year of funding research, is shaping up once again to be immensely productive for Cure Alzheimer’s Fund and our researchers. There is a robust amount of grant applications being submitted by researchers with fascinating hypotheses to explore. We estimate an increase in our funding for research—with a target of $30 million—and as a result will surpass the monumental milestone of distributing $200 million in grants since our inception.

As for the science, there are several areas of research poised for breakthroughs driven by the momentum of prior discoveries, and we are looking forward to seeing what outcomes result. Two such areas of interest are the immune response and biomarkers.

Immune response research investigates the role of neuroinflammation in Alzheimer’s disease. Emerging scientific evidence suggests that in Alzheimer’s disease, the abnormal immune response in the brain is not just the work of the brain’s innate immune system. Immune cells from the periphery, part of the combined innate and adaptive immune system that functions throughout the rest of the body, have been found in the Alzheimer’s brain. Scientists are now looking to better understand this process by asking questions about how these peripheral immune cells enter the brain, why these cells are there and how they may interact with the brain’s innate immune cells to impact Alzheimer’s pathology.

Biomarkers are biological molecules that indicate the presence and potential stage of disease. There has been significant progress in biomarker research for Alzheimer’s disease, but many big questions remain. Novel biomarkers, in addition to amyloid and tau, that can measure other aspects of the disease, like neuroinflammation, neurodegeneration and synapse loss, also are actively being investigated. Predictive biomarkers that identify those at highest risk of future disease long before symptom onset will be a vital tool for making prevention strategies possible.

While we now have amyloid beta and tau biomarkers identified for Alzheimer’s disease that can be measured with positron emission tomography (PET) scans or by sampling cerebrospinal fluid, these tests can be expensive and are not always appropriate for every patient. We now also have blood tests that predict brain amyloid beta. Looking to the future, blood tests that can measure Alzheimer’s disease-related changes in various biomarkers for the disease have the potential to revolutionize diagnosis and staging of the disease.

We are energized by the work that is happening now in these areas of research and in many others, and are committed to sharing what we learn with you.

You make this work possible, and we are looking forward to another incredible year continuing our shared pursuit to gain insights and answers to the questions that will change how we address Alzheimer’s disease.