Our Portfolio

The Alzheimer's Drug Discovery Foundation (ADDF) publishes all programs that we fund in our research portfolio. Funded research projects can be viewed by the year of funding or by program area, and can also be found by searching for an investigator or certain keywords. Please note that your search term(s) must contain at least four characters.

Additionally, please note that grant funding priorities at the ADDF change over time. The ADDF maintains strict confidentiality with all of our funded projects and cannot share additional information on projects without permission from the investigator(s).

The ADDF does not recommend one particular clinical trial or research program over another. The ADDF is not responsible for the accuracy of the information provided, the selection of research subjects (patients) or the conduct of the clinical trial, treatment IND/expanded access program or other research program.

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- Year
- Grantee
- Organization
- Title
- Program Area
- Amount

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- 2017
- Sam Gandy, MD, PhD
- Icahn School of Medicine at Mount Sinai
- Imaging [18F] AV-1451 and [18F] AV-45 in Acute and Chronic Traumatic Brain Injury
- Early Detection, Tau, Neuroimaging, Clinical
- $187,069
Duration: 01/01/2017 - 12/31/2018

Abstract:

Traumatic brain injury (TBI) is a risk factor for chronic traumatic encephalopathy (CTE) and dementia. But our understanding of the long-term effects of TBI is incomplete. Repeated concussions have been associated with an elevated incidence of Alzheimer’s along with a younger age of onset. And brain autopsies of athletes with confirmed CTE have demonstrated tau-containing neurofibrillary tangles and neuropil threads, which are also found in Alzheimer’s patients. But there remains no way to conclusively detect tau and diagnose CTE in living patients. To address this, Dr. Gandy and his team are using PET imaging to investigate amyloid and tau accumulation in subjects with a history of concussions. The investigators are reviewing PET scans along with MRI and neurocognitive data in a cohort of 25 subjects with a history of TBIs and a cohort of 25 subjects with mild cognitive impairment. With this funding, they will add 16 more patients to strengthen their analyses. Their hope is to contribute to the development of biomarkers to diagnose Alzheimer’s and CTE after TBI.

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- 2017
- William Ray, PhD
- The Neurodegeneration Consortium, MD Anderson
- Therapeutic Potential of Dual Leucine Zipper Kinase Inhibitors in Alzheimer’s Disease
- Drug Discovery
- $538,620
Duration: 02/01/2017 - 02/01/2018

Abstract:

When the nervous system sustains an injury, our body eliminates the damaged neurons. Scientists recently discovered that a protein called dual leucine zipper kinase (DLK) regulates this process. Dr. Ray hypothesized that DLK might be abnormally activated in Alzheimer’s disease. He found in several preclinical tests that DLK congregates at sites of neuronal damage early in the disease process and activates genes that trigger neuronal death. DLK inhibitors are a promising approach to treating Alzheimer’s because DLK is only found in neurons and only appears to be active when injury occurs, so inhibiting it won’t affect healthy cells. Dr. Ray and colleagues have already synthesized inhibitors that potently block DLK without disturbing other related genes. In this project, they will optimize their DLK inhibitors to develop a clinical candidate and evaluate its ability to modify disease progression.

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- 2017
- Travis Dunckley, PhD
- Arizona State University
- Testing of Selective DYRK1A Inhibitors as a Novel Treatment for Alzheimer’s
- Drug Discovery, Tau
- $26,401
Duration: 11/01/2017 - 10/31/2018

Abstract:

The accumulation of tau protein into tangles is a hallmark of Alzheimer’s disease. These toxic tangles form when tau is abnormally phosphorylated (or tagged) by enzymes known as kinases. Dr. Dunckley and his colleagues have developed two novel compounds to inhibit DYRK1A, a kinase that phosphorylates tau, as well as other Alzheimer’s-related amyloid proteins. Preliminary data from Dr. Dunckley’s lab indicates that DYRK1A inhibitors safely reduce phosphorylated tau levels in the brain. With this funding, the team will conduct preclinical tests to assess if DYRK1A inhibitors can delay cognitive decline and the onset of Alzheimer’s disease. If successful, the proposed studies will provide critical data to advance one of these drug candidates toward human clinical trials.

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- 2017
- Roberta Diaz Brinton, PhD
- University of Arizona Health Sciences
- Manufacturing of Allopregnanolone
- Clinical
- $450,000
Duration: 06/01/2017 - 05/31/2020

Abstract:

In Alzheimer’s disease, patients lose a significant number of neurons in specific regions of the brain. Scientists assume that regenerating those lost neurons through a process called neurogenesis might restore cognitive function. But previous attempts to spur neurogenesis using stem cells failed. With more than a decade of ADDF funding, Dr. Brinton discovered that the neurosteroid allopregnanolone stimulates the proliferation of stem cells. In preclinical testing, she demonstrated that it did promote neurogenesis, restore cognitive function, and reduce Alzheimer’s pathology in the brain. And a recent phase 1b/2a human clinical trial produced positive findings. Dr. Brinton now plans a larger phase 2 clinical trial. This funding supports the manufacture of allopregnanolone for that trial.

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- 2017
- Richard Mohs, PhD
- Global Alzheimer's Platform Foundation
- A Pilot Project to Enhance Recruitment into Clinical Trials Supported by ADDF
- Clinical
- $100,000
Duration: 11/01/2016 - 11/01/2017

Abstract:

The Global Alzheimer's Platform (GAP) initiative aims to speed up clinical trials of potential Alzheimer’s treatments by improving patient recruitment. Recruitment for Alzheimer’s trials is often slow, leading Phase 2 and 3 trials to take up to 8 years to complete. Recruitment challenges are even greater for trials seeking patients at risk of Alzheimer’s because many don’t know they are at risk. The GAP initiative is working to increase the number of potential study participants developing a comprehensive network around trial sites. Its methods include: volunteer registries; collaborations between health insurers, accountable care organizations, government agencies, and clinical trial sites; and national trial recruitment call centers to screen potential participants. This funding supports the network of GAP clinical sites (GAP-Net) in setting up and using these recruitment resources.

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- 2017
- Christopher Norris, PhD
- University of Kentucky College of Medicine
- Assessment of the Therapeutic Utility of Small Molecule Inhibitors of the Calcineurin/NFAT System
- Drug Discovery, Inflammation, Synaptic Dysfunction
- $257,552
Duration: 11/01/2016 - 11/01/2017

Abstract:

Gene expression is regulated by a complex system, involving many factors. One such factor is NFAT, which works with another factor called calcineurin and is involved in the brain’s immune response and the function of synapses. Overactivation of the NFAT-calcineurin system can lead to neuroinflammation and brain cell death, and it is associated with early stages of Alzheimer’s disease. Current FDA-approved drugs that inhibit calcineurin hold promise as Alzheimer’s treatments, but can cause many adverse side effects. In this project, Dr. Norris will test a novel compound that inhibits NFAT activity, but not calcineurin (the cause of the adverse effects. If preclinical testing shows it to be safer than current drugs, Dr. Norris plans to further develop this compound as a treatment for Alzheimer’s disease.

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- 2017
- Chien-liang Lin, PhD
- The Ohio State University
- Development of Small Molecule Activators of Glutamate Transporter EAAT2 Translation
- Drug Discovery, Synaptic Dysfunction
- $176,156
Duration: 04/01/2017 - 12/31/2017

Abstract:

Glutamate, an amino acid, is an important chemical messenger in the brain. While glutamate is critical for normal brain function, excessive levels can be toxic to brain cells. Normally, glutamate levels are maintained by the EAAT2 protein, which removes excess amounts and prevents glutamate-induced damage in the brain. Loss of the EAAT2 protein is commonly found in Alzheimer's disease patients. Dr. Lin has identified compounds that increase the production of EAAT2. Preliminary studies with one of these compounds restored memory, improved brain cell connections, and reduced levels of beta-amyloid plaques. Over the last two years of ADDF funding, Dr. Lin has made extensive progress in developing compounds with improved drug-like properties. With this funding, he will continue optimizing these compounds and identify the best candidate for human clinical trials. Dr. Lin was previously selected as an ADDF-Harrington Scholar through a partnership with the Harrington Discovery Institute.

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- 2017
- Dominic M. Walsh, PhD
- Brigham & Women's Hospital
- Neurally Derived Exosomes for the Diagnosis and Staging of Sporadic Alzheimer's Disease
- Conferences, Biochemical Biomarkers (Blood, CSF
- $307,782
Duration: 02/01/2017 - 02/01/2019

Abstract:

Recent clinical trials in Alzheimer’s disease have highlighted the need for biomarkers to better diagnose study participants and monitor their response to therapy. Two proteins are strongly linked to Alzheimer’s—tau and beta-amyloid. Current tools—brain imaging and measuring proteins levels in cerebrospinal fluid—can diagnose early symptomatic stages of Alzheimer’s disease but are very expensive and/or painful. Thus, there is an urgent need for less costly and intrusive tests. Recently, researchers discovered that brain cells release small packages called extracellular vesicles, which have contents similar to brain cells. These extracellular vesicles can pass from the brain into the blood and therefore provide a unique opportunity to detect changes occurring in the brain. With this funding, Dr. Walsh will isolate extracellular vesicles from blood and analyze their tau and beta-amyloid levels. The ultimate goal of this work is to develop a simple, inexpensive blood test to diagnose individuals with early stage Alzheimer’s and identify those at risk of developing the disease.

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- 2017
- Steven Finkbeiner, MD, PhD
- The J. David Gladstone Institutes/UCSF
- Utility of Potent Small Molecule Inducers of Autophagy as Potential Agents to Lower Levels of Tau
- Drug Discovery
- $149,002
Duration: 02/01/2017 - 02/01/2019

Abstract:

The abnormal buildup of tau proteins—resulting in toxic tangles—is a hallmark of Alzheimer's disease. One of our brain’s major defenses against accumulating toxic proteins such as tau is a cellular recycling system called autophagy. Treatments that enhance autophagy may help clear excess tau and slow the progression of Alzheimer’s. Dr. Finkbeiner has developed novel small molecules that enhance autophagy in brain cells and may be effective for treating other neurodegenerative diseases such as ALS and Huntington's. With this funding, Dr. Finkbeiner and his colleagues will conduct preclinical tests of the small molecules to further evaluate their potential effectiveness using innovative robotic microscopy developed in the Finkbeiner lab. If successful, he plans to develop the most promising of these small molecules into drugs for later clinical testing.

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- 2017
- Tamara Maes, PhD
- Oryzon Genomics S.A.
- Clinical Development of a Companion Biomarker for the Dual LSD1/MAO-B Inhibitor ORY-2001
- Clinical, Synaptic Dysfunction
- $300,000
Duration: 04/01/2017 - 10/31/2018

Abstract:

Epigenetic mechanisms determine how much a gene is expressed by increasing or decreasing its expression levels, without affecting the underlying genetic code. Prior research has shown that some epigenetic changes—caused by lifestyle factors including stress—have significant effects on genes that control learning and memory and can lead to Alzheimer’s disease. With prior funding from the ADDF, Dr. Maes and her team at Oryzon developed the epigenetic drug ORY-2001, which is now preparing for Phase 2 clinical trials in Alzheimer’s patients. With this funding, Dr. Maes plans to develop a companion biomarker to assess epigenetic changes in human brains. If successful, the effect of ORY-2001 in humans can be monitored by measuring these changes in future clinical trials. This will help identify patients that could benefit most from treatment with ORY-2001 and improve the design and potential success of future clinical trials.

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