Microbial Pathogenesis in Alzheimer’s Disease Grant
Intriguing evidence suggests Alzheimer’s disease may have a link to infectious diseases or a microbial mechanism. Could this be the missing link to lead to a cure for Alzheimer’s disease?
To advance research that could shed light and provide hope to the more than 5.7 million Americans and 47 million people worldwide living with the disease, the IDSA Foundation established the Alzheimer’s Research Grant, now known as the Microbial Pathogenesis in Alzheimer’s Disease Grant, in 2018 to foster further investigation. These grants support research that suggests an infectious agent or microbial community is correlated to Alzheimer’s disease and promotes novel research in the field of microbial triggers for Alzheimer’s disease.
Due to overwhelming interest in this opportunity, the 2023 funding cycle deadline application has been extended to December 23, 2022. Click this link to begin your application.
To read full press release about the Microbial Pathogenesis in Alzheimer’s Disease Grant, click here.
FREQUENTLY ASKED QUESTIONS
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eligibility
- Both members and non-members of IDSA are encouraged to apply. This includes established investigators and academic and health professionals in all disciplines and health-related professions.
- PhDs and MDs are encouraged to apply.
- Interdisciplinary research is encouraged, including collaborations between experts in Alzheimer’s research and infectious diseases.
- Clinical and basic scientists are encouraged to apply.
- International applicants and non-U.S. citizens are eligible to apply.
Anticipated timeline
- February 2023: Grant cycle begins
- August 2023: Interim reports due
- February 2024: Grant cycle ends
To Apply
The application period for the 2023 Microbial Pathogenesis in Alzheimer’s Disease Grant is now open.
For more information:
Contact IDSA Foundation Program Manager Amari Pearson-Fields, PhD, MPH at apearson-fields@idsafoundation.org
about the funders
Alzheimer’s Germ Quest (ALZgerm.org) is a public benefit corporation with the mission of accelerating and deepening investigations into possible microbial causes of Alzheimer’s disease.
The Benter Foundation was founded in 2007 to help communities and individuals thrive. Since then, the Foundation has invested to advance a more livable Pittsburgh, emphasizing the city’s urban core. Reaching beyond Pittsburgh, the Foundation supports peace-building efforts and innovators who create new knowledge to tackle large scale issues. Path-breaking solutions are needed in health challenges like Alzheimer’s disease and opioid abuse. The Benter Foundation believes that the battle against Alzheimer’s will be won through innovative scientific research.
our AWARDEES
In 2021 we awarded more than $1.7 million in grant funds to researchers investigating possible links between infectious diseases and the causation of Alzheimer’s disease. Chosen from among 78 exceptional applications, 11 awardees received grants ranging from $30,000 for fellows or early-career investigators to obtain preliminary data to $250,000 for established investigators who have already developed initial research. The grant funds will be used to initiate or expand their research.
Ilia Baskakov, PhD, professor at the University of Maryland, Baltimore’s Center of Biomedical Engineering and Technology, for his project, “Infectious etiology of late onset Alzheimer’s disease.” Dr. Baskakov will examine the causative relationship between Herpes Simplex Virus 1 (HSV-1) infection of the central nervous system and Alzheimer’s disease using a new mouse model that was generated with the specific purpose of modeling late-onset AD. He will also test whether the role that HSV-1 plays in the etiology of Alzheimer’s disease depends on HSV-1 strain identity. ($250,000)
Elizabeth Bradshaw, PhD, Adler Assistant Professor of Neurology at Columbia University Medical Center, for her project, “Pathogen-driven epigenetic changes in microglia.” Dr. Bradshaw’s hypothesis reasons that infectious processes modify the immune system’s ability to protect the central nervous system (CNS) from neurodegeneration via epigenetic changes in the key AD cell type microglia, the CNS-specific macrophage that is highly implicated in AD. She hypothesizes that a lifetime burden of inflammatory challenges may alter microglial fitness and function. These alterations, compounded in the context of immune aging and suppressive innate immune genetic risk variants, may contribute to disease. This funding will support a better understanding of this process. ($250,000)
Colette Cywes-Bentley, PhD, assistant professor of medicine at Brigham and Women’s Hospital and a 2018 grant recipient, for her project, “Neuroinflammatory impact of microbial material in Alzheimer’s disease.” The key finding from Dr. Cywes-Bentley’s initial AD study that looked at the impact of PNAG vaccination at 5 weeks or 5 months of age in APP-PS1 AD mice showed substantial protection against cognitive deficits and accumulation of beta-amyloid plaques at 12 and 15 months respectively. Her 2021 grant will impact her research and future opportunities for funding by providing the support to explore and extend the results from this initial study to identify the cell types and molecular factors associated with vaccine-induced sparing of cognitive decline. ($250,000)
Pinghui Feng, PhD, MS, professor and chair of the Section of Infection and Immunity at University of Southern California, for his project, “Collateral damage of immune evasion in HSV-1-induced neurodegeneration.” Dr. Feng will dissect the molecular mechanism and determine the functional consequence of HSV-1-induced and aging-associated deamidation of NAMPT in neurodegeneration using an AD mouse model. He believes this research grant will pave the way to harness the findings to prevent and treat neurodegenerative diseases. ($250,000)
Kristen Funk, PhD, assistant professor of biological sciences at University of North Carolina at Charlotte, for her project, “Role of Apobec3 in MHC-I antigen presentation and neuronal synaptic stability in viral neuroinflammation and Alzheimer’s disease.” Dr. Funk hypothesizes that immune response pathways that are activated during viral infection regulate the function of MHC-I proteins that can function in both an immune and neurologic capacity. Results from her studies will define how neuronal MHC-I functions as both a synaptic and immunologic protein, the impact of viral infection on the functional regulation, and one mechanism by which infections may cause the neurocognitive dysfunction associated with Alzheimer’s disease. ($250,000)
Mark Hicar MD, PhD, associate professor of pediatric infectious diseases at University at Buffalo, for his project, “Use of shared antibody responses amongst Alzheimer’s disease patients to reveal an infectious disease etiology.” Dr. Hicar’s research will compare antibodies from Alzheimer’s patients to controls to identify shared antibodies that correlate with having Alzheimer’s disease. The research this grant supports will identify a panel of antibodies specific to Alzheimer’s and initial infectious targets to focus on for future studies. ($100,000)
Xueyi Li, PhD, assistant professor of neurology at Massachusetts General Hospital, for his project, “Vps35 and herpetic virus infection synergy in Alzheimer’s disease.” Dr. Li will examine whether ectopic expression of a single protein of herpetic virus, e.g., gK, along with or without an approach depleting Vps35 in the brain of mice, is sufficient to trigger phenotypes characteristic of Alzheimer’s disease. His goal is to delineate a cause-effect role for herpetic virus in the development of Alzheimer’s disease and to unveil cell surface proteins affected by herpetic virus in neurons. ($100,000)
Jason Tchieu, PhD, assistant professor of developmental biology at Cincinnati Children’s Hospital Medical Center, for his project, “Investigating the impact of the endogenous retrovirus HERV-K(HML-2) in Alzheimer’s disease.” Dr. Tchieu will explore how human endogenous retroviruses (HERVs) can contribute to neurodegeneration. This funding will be used to determine what genes are regulated by HERVs and whether similar genes are differentially regulated in Alzheimer’s disease. He predicts that HERV activity could modulate cellular states leading to increased stress or alter metabolic profiles, which are both factors important in neurodegeneration. ($100,000)
Richard Thompson, PhD, professor of molecular genetics, biochemistry and microbiology at University of Cincinnati College of Medicine, for his project, “Iron and the intersection of herpes simplex virus infection, the human ApoE4 allele and Alzheimer’s disease.” Dr. Thompson will examine the idea that HSV infection of neural tissues in the context of huApoE4 leads to increased iron-induced oxidative injury, exacerbating the initiation and progression of AD. The model being developed will permit the testing of basic hypotheses such as whether and when post-infection antiviral treatments may reduce or eliminate evidence of cognitive dysfunction. ($100,000)
Ravinder Nagpal, PhD, assistant professor of nutrition and integrative physiology at Florida State University, for his project, “Klebsiella pneumoniae as a microbial trigger for Alzheimer’s disease: from microbial pathogenesis to neuropathogenesis.” Dr. Nagpal will investigate if there is a role for Klebsiella pathogenesis in Alzheimer’s neuropathogenesis. If so, then he will explore what mechanisms are involved therein. If found true, these findings will provide a new line of evidence to prove his hypothesis that Alzheimer’s disease does have a link to infectious diseases or a microbial mechanism, thereby paving the way for further larger studies to address Alzheimer’s from an infectious diseases perspective. ($30,000)
Kevin Zwezdaryk, PhD, assistant professor of microbiology and immunology at Tulane University, for his project, “The role of infectious agent-driven mitochondrial dysfunction in Alzheimer’s disease.” Dr. Zwezdaryk will test the hypothesis that infection impacts brain aging by altering mitochondrial function and energy production. He hopes to gain insights into the relationship of infection, age and AD, permitting the discovery of novel strategies to prevent or treat AD. ($30,000)
Laura Cox, Ph.D., instructor in Neurology at the Brigham and Women’s Hospital, Harvard Medical School, Boston, for her research “Investigating Strain-Specific Pathogenicity Factors in Bacteroides that Influence Alzheimer’s disease.” Dr. Cox’s research will characterize B. fragilis strains from AD patients and healthy controls, then test whether AD-strains have enhanced capacity to contribute to AD pathogenesis using in vivo and in vitro systems. These studies have the potential to identify molecular targets in Bacteroides fragilis that could one day be used to develop diagnostic screening tests and novel therapeutic approaches for Alzheimer’s disease.
Daniel Czyz, Ph.D., assistant professor at the University of Florida, Gainesville, for his research “Deciphering the Effect of Human Microbiota on Alzheimer’s Disease Using C. Elegans.” Dr. Czyz will employ Caenorhabditis elegans as a model to determine how various bacteria from the human microbiome affect protein folding in the host, and what are the underlying mechanisms. He anticipates his research will reveal results that are crucial to the development of Alzheimer’s disease diagnostics and therapeutics.
Gautam Dantas, Ph.D., professor at Washington University School of Medicine, St. Louis, for his research “Investigating Gut Microbiome Composition and Functions During Stages of Alzheimer’s Disease.” Changes in the human gut microbiome have been reported in individuals with symptomatic AD. Dr. Dantas hypothesizes these changes occur very early in the disease process, during the “preclinical” stage of AD, when neurological biomarkers are present, but the individual still has normal cognition. If true, detecting microbial species would be cheaper and faster than current methods for diagnosing the earliest changes seen with AD and could provide new potential targets to treat/prevent AD.
Eran Elinav, M.D, Ph.D., principal investigator at the Weizmann Institute of Science, Israel, for his research “Decoding Microbial Species and Products Modulating Alzheimer’s Disease Towards Precision Probiotics and Postbiotics Treatment.” Dr. Elinav’s research hypothesizes that individualized compositional and/or functional microbiome alterations in the gut may have causal impact on AD. Dr. Elinav will study how the microbiome affects AD development, attempting to identify and characterize beneficial versus disease-associated microbiome, and how changes in bacterial composition or metabolites may affect the brain function in an AD murine model. By utilizing state-of-the-art microbiome technologies, we aim to shed new light on host-microbiome regulation of normal and AD-prone brain function, so to identify new therapeutic targets against Alzheimer’s disease.
Bert Jacobs, Ph.D., professor at Arizona State University, Tempe, for his research “The Role of Microbe-induced Necroptotic Death in Tauopathy.” Dr. Jacobs will test his hypothesis that recruitment of tau to stress, or virus-induced granules can lead to necroptotic cell death. He plans to ask if introduction of pathogenic tau in the brains of mice is leading to necroptotic death in neurons, and if introduction of a virus that can lead to induction of necroptotic cell death can increase pathology induced by pathogenic tau.
Abhay Moghekar, M.B.B.S., associate professor at Johns Hopkins University, Baltimore, for his research “Meta-omics to Unravel Microbial Landscape During the Full Spectrum of Alzheimer’s Disease.” Dr. Moghekar hopes to identify the altered brain-linked microbial and, or host protein/peptides signatures in this study which will represent a first step towards exploring microbial signatures in CSF of subjects with Alzheimer’s disease. The meta-omics data will provide much-needed support for ͞microbial hypothesis͟ and help in better understanding of the relationship between microbial gene copy number and protein abundance during the progression of AD. The research proposed will generate pilot data that will pave the way for future studies correlating longitudinal cohorts with the appearance of microbial signatures in the CSF with classical neurodegenerative (amyloid and tau) and neuroinflammatory (sTREM2, IL10) markers explored in new submissions.
Ashley Moseman, Ph.D., assistant professor at Duke University School of Medicine, Durham, for his research “Infectious Influence: Using Fate Mapping to Determine how Sites of Historical Viral Infection Impact Alzheimer’s Disease Initiation.” Dr. Moseman has developed an infectious neurotropic virus that expresses Cre-recombinase. When this virus infects the brain, it can label permanently infected cells that are cleared of virus and survive infection. This permanent label allows his research to specifically localize areas of former viral infection. In this study he will infect 5xFAD AD model mice with the Cre expressing viruses to colocalize amyloid beta deposition and glial activation with previously infected regions and correlate these changes with behavioral evidence of AD acceleration.
Nancy Sawtell, Ph.D., professor at Cincinnati Children’s Hospital Medical Center, Cincinnati, for her research “Is Pathogen-Initiated Tau Seed Propagation from Peripheral to Central Nervous System an Early Event in the Development of Late Onset Alzheimer’s Disease.” Dr. Sawtell will Use HSV engineered viruses to test the hypothesis that viral reactivation events in the PNS promote axonal transport of toxic tau variants from the PNS into the CNS. Transport of tau seeds into the CNS would lead to their propagation and spread within the brain in a prion-like manner, accelerating the damage that leads to LOAD. If true, current antiviral treatments may be of great use in preventing or inhibiting the progression of LOAD.
Christoph Thaiss, Ph.D., assistant professor at the University of Pennsylvania, Philadelphia, for his research “Microbial Control of Amyloid Precursor Protein.” Several scientific theories have been generated to explain the pathogenesis of Alzheimer’s disease. Among the most prominent theories are the amyloid theory, which focuses on the role of amyloid proteins in the brain, and the infectious hypothesis, which focuses on the role of microorganisms. Dr. Thaiss aims at combining both theories into a unified concept, whereby microbial regulation of amyloid proteins may be a critical component of the development of Alzheimer’s disease. He will use a combination of technologies from the fields of microbiology, gnotobiology and neuroscience to determine a pathway that links microorganisms to the biology of amyloid proteins.
Kyle Walsh, Ph.D., associate professor at Duke University School of Medicine, Durham, for his research “Serologic and Genomic Modifiers of Beta-Amyloid Levels in an Immuno-Compromised Cohort of Adult Down Syndrome Patients.” Dr. Walsh will test his hypothesis that evaluation of the relationship between infection history and early markers of Alzheimer’s disease in an “extreme phenotype” cohort of Down Syndrome patients will accelerate research into the infectious etiology of AD. To address his research questions, his research will evaluate the viral infection history of these individuals to gain new insights into the interaction between genetic variation and infection history in DS-associated AD pathogenesis, subsequently translating insights to AD prevention in the general population.
Mujeeb Salaam, Ph.Dc., MPH, MSc, a researcher at the Islamic University in Uganda, for his research “HIV/AIDS, Syphilis, Cardiovascular Diseases as Predisposing Factors to Dementia Among Patients Attending Selected Referral Hospitals in Uganda” was awarded the $8,000 pilot grant. “Funding is a major challenge to quality research in Africa, I am so excited to be given the opportunity to showcase our ability to conduct good research that can solve human problems and alleviate human sufferings. HIV/AIDS and Syphilis prevalence in Uganda is much higher compared to other western countries, the findings from this research might suggest having different prevalent rates for Alzheimer’s disease in Africa,” said Dr. Mujeeb Salaam.
Maria Eugenia Ariza, PhD, Assistant Professor at The Ohio State University, Columbus
“Role of the Herpesvirus dUTPase Proteins in Late-Onset Alzheimer’s Disease (LOAD).”
Alberto Costa, MD, PhD, Professor at Case Western Reserve University, Cleveland
“Is the Amyloid-Beta Peptide a Necessary Element in Preventing the Spread of Porphyromonas gingivalis Infection in the Brain?”
Jason Grayson, PhD, Associate Professor, Wake Forest School of Medicine, Winston-Salem, N.C.
“Using Machine Learning to Determine the Role of Herpesvirus-Specific CD8+ T Cells in Alzheimer’s Disease.”
Catherine Helmer, PhD, Permanent Researcher at Bordeaux University, France
“Viral Infections in Alzheimer’s Disease (VirAlz).”
Marvin K. Schulte, PhD, Professor and Department Chair at Idaho State University, Pocatello, ID
“Viral Mimicry in Alzheimer’s Disease.”
Colette Cywes-Bentley, PhD, Brigham & Women’s Hospital, Harvard Medical School
“The Role for Pathogen Expressed PNAG in Alzheimer’s Disease.”
Allison Aiello, PhD, MS, University of North Carolina, Chapel Hill
“The Role of Dementia-Associated Pathogen Burden in the Development of Alzheimer’s Disease (AD) and Other Dementias.”