Episode 580: Can Treating Lyme Disease Reverse Alzheimer’s Biomarkers? Dr. Richard Horowitz’s New Study

Could Lyme disease and other chronic inflammatory triggers play a role in Alzheimer’s disease—and could addressing those underlying factors change measurable Alzheimer’s biomarkers?

In this episode of the Tick Boot Camp Podcast, Dr. Richard Horowitz returns to discuss a provocative new case report he published exploring the relationship between Lyme disease, neuroinflammation, Alzheimer’s disease biomarkers, and dapsone combination therapy.

The conversation centers on a patient with a long history of Lyme disease who had an elevated phosphorylated tau 217 (p-tau217) level, an increasingly important blood biomarker associated with Alzheimer’s disease. After completing a nine-week dapsone combination protocol, the patient’s p-tau217 declined by approximately 63% and returned to the normal range. Her amyloid-beta 42/40 ratio also moved in a favorable direction, and she reported improved cognitive clarity.

This case provides a new research question: Could infections, toxins, metabolic dysfunction, sleep disorders, microbiome disturbances, and other inflammatory drivers contribute to Alzheimer’s pathology in subsets of patients—and could identifying and addressing those drivers change the course of the disease?

Read the Published Study

Read Dr. Horowitz’s published study on SAGE Journals

The case report provides the scientific foundation for much of the discussion in this episode, including the changes in p-tau217 and amyloid biomarkers following treatment.

In This Episode, You’ll Learn

Lyme Disease and Alzheimer’s Disease

Dr. Horowitz reviews research that has investigated possible relationships between Borrelia burgdorferi, neuroinflammation, amyloid, phosphorylated tau, and Alzheimer’s pathology.

Much of the earlier work examining spirochetes and Alzheimer’s disease involved brain tissue and postmortem studies. Dr. Horowitz explains why he believes studying Alzheimer’s biomarkers in living Lyme disease patients may provide another way to investigate these questions.

The discussion also explores an important distinction: finding an association between infection and Alzheimer’s pathology does not mean every case of Alzheimer’s disease is caused by Lyme disease.

The Patient Who Sparked the New Case Report

Dr. Horowitz describes a longtime patient with Lyme disease whose p-tau217 was substantially elevated despite her perception that her cognition was relatively good.

After the patient underwent his nine-week dapsone combination protocol, repeat testing showed a substantial reduction in p-tau217, bringing the biomarker into the normal range.

Dr. Horowitz also discusses changes in the patient’s amyloid-beta 42/40 ratio, rheumatoid factor, and subjective cognitive function.

The case led him to ask whether treatment directed at persistent infection and inflammation could influence biomarkers normally associated with Alzheimer’s disease.

What Is p-Tau217?

A major portion of the interview focuses on the emerging use of blood-based biomarkers for evaluating Alzheimer’s pathology.

Dr. Horowitz discusses four primary biomarkers:

• p-tau217 – phosphorylated tau 217
• p-tau181 – phosphorylated tau 181
• Amyloid-beta 42/40 ratio
• Neurofilament light chain (NfL)

He also discusses GFAP (glial fibrillary acidic protein) and the potential relevance of APOE genetics.

Dr. Horowitz describes p-tau217 as one of the most sensitive and specific currently available blood biomarkers associated with Alzheimer’s disease pathology.

Amyloid May Be More Than Just “Plaque”

Why does amyloid accumulate in the brain in the first place?

The episode explores the concept of amyloid-beta as an antimicrobial peptide and the hypothesis that amyloid production may, in some circumstances, be part of the brain’s response to biological threats.

Dr. Horowitz discusses research examining potential infectious and environmental contributors to amyloid production, including:

• Borrelia and other bacteria
• Viral infections
• Fungal organisms
• Other microbes
• Environmental toxins

The conversation then explores how a response that may initially be protective could potentially become harmful when amyloid accumulates and interferes with normal neuronal function.

Amyloid, Tau and Neurodegeneration

Dr. Horowitz breaks down two major features associated with Alzheimer’s disease.

Amyloid-beta plaques accumulate outside neurons and are associated with disrupted communication between brain cells.

Tau proteins normally help stabilize structures inside neurons. Abnormally phosphorylated tau can become associated with neuronal dysfunction and neurodegeneration.

The discussion also explores why some patients may have abnormal tau biomarkers without corresponding abnormalities in amyloid markers—and why much more research is needed to understand these patterns in people with chronic Lyme disease.

Dapsone Combination Therapy and Cognitive Symptoms

Dapsone has been a major focus of Dr. Horowitz’s research into persistent Lyme disease.

In this episode, he explains that his protocols involve combination therapy rather than dapsone alone and discusses his previous published work examining dapsone combination therapy in patients with persistent Lyme disease symptoms.

According to Dr. Horowitz, improvements in memory, concentration, cognition, and word-finding difficulties have repeatedly been among the most notable improvements reported in his patient cohorts.

He believes this observation deserves greater attention now that blood-based Alzheimer’s biomarkers make it possible to investigate biological changes alongside cognitive symptoms.

Dapsone, the Brain and the NLRP3 Inflammasome

The discussion goes beyond dapsone’s antimicrobial activity.

Dr. Horowitz explains his interest in the NLRP3 inflammasome, an inflammatory pathway implicated in neuroinflammation and studied in relation to Alzheimer’s disease.

He proposes that dapsone could potentially have more than one relevant effect—targeting certain microorganisms as part of combination therapy while also influencing inflammatory pathways.

This remains an area requiring further clinical investigation.

Alzheimer’s Disease May Have Multiple Drivers

One of the most important themes of the interview is that Alzheimer’s disease is unlikely to have a single universal cause.

Dr. Horowitz applies his 16-point MSIDS (Multiple Systemic Infectious Disease Syndrome) model to cognitive decline and Alzheimer’s disease.

Potential contributors discussed include:

• Lyme disease and other infections
• Mold and mycotoxin exposure
• Heavy metals and environmental toxins
• Chronic inflammation
• Insulin resistance and blood sugar dysregulation
• Sleep disorders and sleep apnea
• Gut microbiome dysfunction
• Nutritional deficiencies
• Mitochondrial dysfunction
• Cardiovascular and metabolic factors
• Other sources of systemic inflammation

Rather than focusing exclusively on amyloid or tau, Dr. Horowitz argues for investigating what may be driving those abnormalities in an individual patient.

Lyme Disease Is Not the Only Possible Infectious Trigger

The episode also examines the broader question of infection and neurodegeneration.

Dr. Horowitz discusses scientific literature investigating organisms and infections beyond Borrelia, including Chlamydia pneumoniae, Helicobacter pylori, Coxiella burnetii, herpesviruses, and other microbial exposures.

His central argument is not that every Alzheimer’s patient has an infection. Instead, he believes clinicians and researchers should investigate whether infectious, toxic, metabolic, environmental, and inflammatory factors may coexist and contribute differently from patient to patient.

The Challenge of Lyme Disease Testing

The conversation also addresses limitations surrounding Lyme disease diagnostics.

A negative standard Lyme disease test does not necessarily answer every clinical question surrounding prior exposure or persistent symptoms. The hosts and Dr. Horowitz discuss why testing methodology, timing, immune response, strain diversity, clinical history, and other factors may need to be considered when evaluating a complex patient.

Dr. Horowitz also explains how he combines laboratory findings with clinical history and his MSIDS framework when evaluating patients.

Why More Data Is Critical

A single case can generate a hypothesis. It cannot establish a treatment standard.

Dr. Horowitz repeatedly emphasizes the need for:

• Additional documented cases
• Standardized biomarker testing
• Long-term patient follow-up
• Larger patient cohorts
• Collaboration among Lyme-literate physicians and neurologists
• Shared research databases
• Multicenter studies
• Randomized controlled clinical trials

The episode explores the possibility of physicians systematically collecting Alzheimer’s biomarkers before and after treatment of specific MSIDS factors to determine which interventions, if any, consistently change those biomarkers.

That type of data could help researchers move beyond individual clinical observations toward testable conclusions.

Could Patient Data Accelerate Lyme and Alzheimer’s Research?

Matt and Dr. Horowitz discuss the potential for a secure research repository where physicians could contribute standardized patient data.

For example, researchers could track a patient’s infections, mold exposure, metabolic factors and other MSIDS variables alongside p-tau217, p-tau181, amyloid-beta 42/40 and NfL measurements.

Repeating those measurements after individual interventions could help researchers identify patterns that would otherwise take years to discover through isolated clinical practices.

Dr. Horowitz Is Developing an MSIDS App

Dr. Horowitz also shares a major project currently in development.

He says he is working with researchers from the University of California, Irvine on an application designed to translate his MSIDS framework into a digital tool.

The goal is for users to enter information based on the MSIDS questionnaire and other health data, allowing the software to help guide them through the framework.

Dr. Horowitz also discusses how a sufficiently large and secure database could eventually create opportunities for collecting real-world patient data and generating new research hypotheses.

Lifestyle, Metabolic Health and Brain Health

Not every potential driver discussed in this episode is infectious.

Dr. Horowitz highlights several established areas of brain-health research, including:

• Mediterranean/MIND-style dietary patterns
• Regular physical activity
• Healthy blood sugar and insulin regulation
• Cardiovascular health
• Adequate sleep
• Addressing sleep apnea
• Omega-3 fatty acids
• Nutritional status
• Gut and microbiome health

This reinforces one of the episode’s central messages: cognitive decline may result from multiple interacting biological pressures rather than one isolated mechanism.

Ending Chronic Illness

The discussion also previews Dr. Horowitz’s upcoming book, Ending Chronic Illness, scheduled for publication on October 13, 2026.

The book expands on his 16-point MSIDS model and explores how overlapping infectious, inflammatory, environmental, metabolic, immune, neurological, and lifestyle factors may contribute to chronic disease.

A separate Tick Boot Camp interview dedicated to the new book will be released this fall.

Learn More About Dr. Richard Horowitz

Dr. Richard Horowitz is one of the best-known physicians in the Lyme disease community and has spent decades treating patients with Lyme disease, tick-borne infections, and complex chronic illness.

Tick Boot Camp has interviewed Dr. Horowitz multiple times about Lyme disease, Babesia, Bartonella, dapsone combination therapy, MSIDS, chronic inflammation, and emerging research.

Visit Dr. Richard Horowitz’s Tick Boot Camp page for all of our interviews, articles, and resources

Additional Resources

Explore all Tick Boot Camp interviews and information

Key Topics

Richard Horowitz, MD; Lyme disease; Alzheimer’s disease; Alzheimer’s biomarkers; Lyme disease and Alzheimer’s; Lyme disease and dementia; cognitive decline; neuroinflammation; p-tau217; p-tau181; phosphorylated tau; amyloid beta; amyloid-beta 42/40 ratio; neurofilament light chain; NfL; GFAP; APOE4; Borrelia burgdorferi; chronic Lyme disease; persistent Lyme disease; dapsone; dapsone combination therapy; MSIDS; Multiple Systemic Infectious Disease Syndrome; biofilms; persister bacteria; brain inflammation; memory problems; brain fog; cognitive dysfunction; mold toxicity; mycotoxins; microbiome; infections and Alzheimer’s disease; tick-borne disease; Lyme disease research; dementia research; Alzheimer’s research.