Can Lyme Disease Be Mistaken for Dementia? Brain Fog, Memory Loss, and Alzheimer’s

Lyme disease may cause memory loss, confusion, and brain fog
Rare cases can produce dementia-like cognitive decline
Lyme disease has not been established as a cause of Alzheimer’s disease

Can Lyme disease cause dementia? Lyme disease is not an established cause of Alzheimer’s disease or other primary neurodegenerative dementias. However, Lyme neuroborreliosis can produce cognitive symptoms—including brain fog, memory loss, confusion, and slowed thinking—that may resemble dementia. Rare cases of dementia-like cognitive decline associated with Lyme neuroborreliosis have also been reported.

This distinction is important. A dementia-like syndrome associated with neurologic Lyme disease is different from Alzheimer’s disease or Lewy body dementia. Published cases show that Lyme neuroborreliosis can occasionally produce substantial cognitive decline, sometimes with improvement after antibiotic treatment. At the same time, population studies have not demonstrated an increased long-term risk of dementia or Alzheimer’s disease following Lyme neuroborreliosis.^2,4,5,8,9

A 2025 clinical practice guideline on potentially treatable causes of cognitive impairment specifically includes Lyme disease among neuroinfectious conditions clinicians may consider during the evaluation of potentially reversible dementia-like syndromes.⁷

Meanwhile, researchers continue to investigate a different question: whether microbes might contribute to biological pathways involved in Alzheimer’s disease. A 2024 review examined evidence involving bacteria, viruses, fungi, and protozoa and included Borrelia burgdorferi among the organisms that have been studied.¹⁰ That research is intriguing, but it does not establish that Lyme disease causes Alzheimer’s disease.

The distinction matters. Lyme neuroborreliosis appears to be an uncommon explanation for dementia-like cognitive decline. But when cognitive decline is atypical, progresses unusually rapidly, fluctuates, occurs with other neurologic or systemic symptoms, or develops in someone with plausible tick exposure, Lyme disease may belong in the differential diagnosis.

I’ve spent much of my career studying cognitive decline. Before I specialized in Lyme disease, I taught medical students about dementia and ran programs evaluating memory loss in older adults. So when I say that Lyme disease and dementia can sometimes be confused, I don’t say it lightly.

One of my patients was referred to me with a working diagnosis of dementia. He had memory issues, word-finding problems, and trouble concentrating. But the timeline did not quite add up. He was not deteriorating in the typical way. He had a history of outdoor exposure—and no one had considered Lyme disease.

Following treatment for Lyme disease, his cognitive symptoms improved substantially. He eventually returned to working part-time and enjoying life.

Lyme disease can sometimes be mistaken for dementia when brain fog, memory loss, confusion, and slowed thinking dominate the clinical picture. A careful evaluation is important because some causes of cognitive decline are potentially treatable.

Why Lyme Disease Can Be Mistaken for Dementia

Lyme disease and dementia can share symptoms involving memory, concentration, language, and thinking.

Symptoms reported with Lyme-related cognitive dysfunction may include:

• Brain fog
• Short-term memory problems
• Difficulty concentrating
• Word-finding problems
• Confusion
• Mood changes or irritability
• Slowed processing speed
• Difficulty completing familiar tasks
• Fatigue that worsens cognitive function

These symptoms can overlap with mild cognitive impairment, Alzheimer’s disease, depression, sleep disorders, medication effects, and many other medical conditions. Cognitive symptoms alone therefore cannot establish Lyme disease.

Lyme-related cognitive complaints may sometimes fluctuate or occur alongside fatigue, headaches, pain, neuropathy, dizziness, or other neurologic symptoms. A pattern that is unusual for a primary neurodegenerative disorder may provide a reason to investigate alternative causes.

Lyme Disease and Dementia: Know the Difference

Dementia is a clinical syndrome involving cognitive decline severe enough to interfere with independent daily functioning. Alzheimer’s disease is the most common cause of dementia and typically progresses gradually over time.

Lyme disease can cause cognitive impairment, but it does not usually behave like a primary neurodegenerative dementia.

Features that may prompt consideration of Lyme disease or another secondary cause include:

• Sudden, subacute, rapidly progressive, or fluctuating cognitive symptoms
• Cognitive changes occurring with headaches, neuropathy, dizziness, gait problems, joint pain, or other neurologic or systemic symptoms
• Possible tick exposure or residence or travel in an endemic area
• A history of an expanding rash or other manifestations compatible with Lyme disease
• Neurologic findings not readily explained by a typical dementia syndrome
• A clinical course that does not follow the expected pattern of Alzheimer’s disease

None of these findings proves Lyme disease. They indicate that clinicians may need to look beyond a primary neurodegenerative diagnosis.

Lyme Disease Memory Loss

Patients with Lyme disease may describe cognitive difficulties differently from the progressive memory loss typically associated with Alzheimer’s disease.

Some report losing words, forgetting why they entered a room, struggling to follow conversations, having difficulty multitasking, or needing substantially more effort to complete mentally demanding tasks.

Others describe a “mental fog” rather than complete loss of stored memories. They may know what they want to say but have difficulty retrieving the word or organizing the thought.

These problems may occur together with fatigue, sleep disturbance, pain, headaches, dizziness, or other neurologic symptoms.

These features are not unique to Lyme disease. Similar cognitive complaints can occur with many medical, neurologic, psychiatric, sleep, and postinfectious conditions.

Lyme Brain Fog vs. Alzheimer’s Disease

Not every case of brain fog is Alzheimer’s disease, and not every older adult with memory problems has dementia.

Lyme-related brain fog may involve slowed thinking, difficulty concentrating, word-finding problems, forgetfulness, and reduced mental stamina. Alzheimer’s disease more typically causes progressive impairment in memory and other cognitive domains that increasingly interferes with independent function.

There can be considerable overlap in the way patients describe their symptoms. That is why the diagnosis should not be based on a symptom checklist alone.

When cognitive symptoms occur alongside neurologic or systemic complaints and a history compatible with tick exposure, Lyme disease may be one of several conditions considered during the evaluation.

Can Lyme Disease Cause Dementia-Like Symptoms?

Yes, but this appears to be uncommon. Lyme neuroborreliosis has been reported to produce dementia-like cognitive syndromes in some patients.^2-5

The phrase “dementia-like” is important. Lyme disease has not been established as a cause of Alzheimer’s disease, Lewy body dementia, frontotemporal dementia, or other primary neurodegenerative dementias.

A 2024 review of Lyme neuroborreliosis in the context of dementia syndromes concluded that dementia-like syndrome is an infrequent manifestation of Lyme disease and that the literature does not provide sufficiently convincing evidence linking Borrelia infection with primary dementia syndromes.⁵

However, secondary dementia-like syndromes associated with Lyme neuroborreliosis have been described. Distinguishing these uncommon presentations from primary neurodegenerative disease requires careful clinical assessment.

What Do Documented Cases of Lyme-Related Dementia Look Like?

Kristoferitsch and colleagues reviewed patients with secondary dementia associated with Lyme neuroborreliosis.⁴ The clinical pattern differed in important ways from typical primary neurodegenerative dementia.

The dementia developed relatively rapidly, reaching a moderate stage within approximately 6 to 12 months. Other findings could include gait abnormalities and additional neurologic or systemic symptoms. Cerebrospinal fluid findings supported an inflammatory neurologic process, including pleocytosis, elevated protein, and intrathecal production of antibodies against Borrelia in well-documented cases.⁴

Importantly, improvement following antibiotic treatment was reported. This supports the concept of a secondary dementia-like syndrome due to Lyme neuroborreliosis rather than Alzheimer’s disease being reversed by antibiotics.

The distinction is clinically important because a rapidly developing or otherwise atypical dementia syndrome may warrant evaluation for potentially treatable neurologic, infectious, metabolic, inflammatory, or structural causes.

Does Lyme Disease Increase the Risk of Alzheimer’s Disease?

There is currently insufficient evidence to conclude that Lyme disease causes Alzheimer’s disease or increases an individual’s risk of developing it.

A large Danish population-based study compared 2,067 patients with Lyme neuroborreliosis with 20,670 age- and sex-matched individuals from the general population.⁹ The investigators found no long-term increased risk of dementia or Alzheimer’s disease among patients with Lyme neuroborreliosis.

Wormser and colleagues also reviewed evidence concerning Lyme disease, Alzheimer’s disease, and Lewy body dementia and concluded that convincing evidence was lacking that Lyme disease causes either primary neurodegenerative disorder.⁸

These findings are important because they distinguish the uncommon dementia-like syndromes reported with active neurologic Lyme disease from the much broader claim that Lyme disease causes Alzheimer’s disease.

What About Lewy Body Dementia?

A published case raised the possibility that Borrelia burgdorferi might be associated with Lewy body dementia after borrelial material was reported in postmortem tissue.⁸

Wormser and colleagues challenged that interpretation, citing concerns about the clinical history, laboratory methods, PCR findings, controls, and the possibility of laboratory contamination.⁸

The available evidence therefore does not establish Lyme disease as a cause of Lewy body dementia.

This does not negate the ability of Lyme neuroborreliosis to cause neurologic and cognitive illness. Rather, it reinforces the need to distinguish secondary cognitive impairment associated with Lyme disease from a primary neurodegenerative disorder.

Researchers Are Still Studying Microbes and Alzheimer’s Disease

Researchers have been investigating a broader question: could microbes contribute to some of the biological processes involved in Alzheimer’s disease?

Williams and colleagues reviewed evidence involving bacteria, viruses, fungi, protozoa, the gut microbiome, and oral microorganisms. The proposed mechanisms include chronic inflammation, immune activation, disruption of biological barriers, and interactions with processes involved in amyloid and tau pathology.¹⁰

Borrelia burgdorferi was among the organisms discussed. Previous studies cited by the review have reported Borrelia-associated findings in Alzheimer’s brain tissue and experimental changes involving amyloid-beta and phosphorylated tau after exposure to Borrelia.¹⁰

These observations are biologically interesting, but they do not answer the clinical question of whether Lyme disease causes Alzheimer’s disease.

Finding an organism or microbial material in tissue does not by itself demonstrate that the organism caused the neurodegenerative process. Likewise, demonstrating changes in amyloid or tau in an experimental system does not establish that the same process causes Alzheimer’s disease in people with Lyme disease.

The direction of the relationship is also uncertain. Microbes might contribute to inflammation or other disease processes, but changes associated with aging or neurodegeneration might also make the brain more vulnerable to microbial entry or persistence. Both processes could potentially occur together.

For now, the most defensible conclusion is that the microbial hypothesis of Alzheimer’s disease remains an active area of research, while a causal relationship between Lyme disease and Alzheimer’s disease has not been established.¹⁰

Why Lyme Dementia-Like Illness and Alzheimer’s Research Should Not Be Confused

Two very different questions are often blended together.

The first is whether Lyme neuroborreliosis can occasionally cause cognitive impairment severe enough to resemble dementia. Published clinical cases and series indicate that it can.^2-5

The second is whether infection with Borrelia burgdorferi contributes to the development of Alzheimer’s disease itself. That remains unproven.^5,8-10

A patient improving cognitively after treatment for Lyme neuroborreliosis therefore does not demonstrate that Alzheimer’s disease was cured with antibiotics. The more appropriate interpretation may be that an infectious or inflammatory neurologic syndrome had been mimicking a primary dementia.

This distinction prevents both extremes: overlooking a potentially treatable infection in an appropriate patient and attributing primary neurodegenerative dementia to Lyme disease without sufficient evidence.

2025 Guideline Includes Lyme Among Potentially Treatable Causes of Cognitive Impairment

A 2025 clinical practice guideline on cognitive impairment in treatable dementias reinforces the importance of searching for secondary causes before assuming that cognitive decline is irreversible.⁷

The guideline includes Lyme disease among neuroinfectious disorders associated with potentially reversible cognitive impairment. It lists clinical clues that may accompany Lyme disease, including headache, fever or feverishness, muscle and joint pain, numbness, tiredness, and signs of meningitis.⁷

The guideline also includes Borrelia antibody testing among investigations that may be considered when the clinical presentation raises suspicion for Lyme disease.⁷

This does not mean that everyone with memory loss should automatically be tested for Lyme disease. Testing is most useful when interpreted in the context of symptoms, exposure history, examination findings, geographic risk, and the overall clinical picture.

Potentially Treatable Does Not Mean Dementia Usually Reverses

The 2025 guideline makes another important distinction. Identifying a potentially reversible cause of cognitive impairment does not guarantee that established dementia will completely disappear with treatment.⁷

The authors cite a meta-analysis in which potentially reversible causes were identified in approximately 9% of patients evaluated for dementia, while actual reversal of dementia occurred in only about 0.6%.⁷

That distinction is particularly important when discussing Lyme disease. Published cases show that Lyme neuroborreliosis can occasionally produce cognitive syndromes that improve with treatment, but they do not establish that Lyme disease is a common explanation for dementia or that cognitive decline will necessarily reverse after antibiotics.

What Does the Lyme Medical Literature Show?

The Lyme-specific literature includes case reports, case series, observational studies, reviews, and studies of cognitive impairment associated with neurologic or previously treated Lyme disease.

Blanc and colleagues evaluated 1,594 patients referred for dementia and identified 20 with evidence of intrathecal Borrelia antibody production. Seven were ultimately considered to have Lyme neuroborreliosis. Their cognitive symptoms remained stable or improved following antibiotic treatment.²

The other 13 patients were ultimately diagnosed with primary neurodegenerative or vascular disorders, including Alzheimer’s disease, Lewy body disease, frontotemporal lobar degeneration, hippocampal sclerosis, and vascular dementia despite their positive Lyme-related findings.²

This illustrates a critical point: positive Lyme testing alone does not prove that Lyme disease is responsible for cognitive decline. Laboratory findings must be interpreted within the complete clinical picture.

Sanchini and colleagues reported a 75-year-old man admitted to an Alzheimer’s disease care unit with hallucinations, confusion, and aggressive behavior. His Borrelia burgdorferi serology was positive and confirmed by immunoblot. He declined cerebrospinal fluid examination but experienced marked clinical improvement after antimicrobial treatment. The authors described Lyme disease as an uncommon cause of reversible dementia.³

Case reports can illustrate what is clinically possible, but they cannot establish how frequently this occurs or prove that Lyme disease explains cognitive decline in other patients.

What About Cognitive Problems After Lyme Disease Treatment?

Cognitive symptoms are not limited to patients presenting with a classic dementia-like syndrome.

Fallon and colleagues studied 37 patients with well-documented Lyme disease, previous antibiotic treatment, positive IgG Western blot, and objective memory impairment.⁶ Participants received 10 weeks of intravenous ceftriaxone or placebo.

The antibiotic-treated group had moderate short-term cognitive improvement at week 12, but the cognitive benefit was not sustained at week 24 after treatment had ended.⁶

This study demonstrates that measurable cognitive impairment can occur in patients with previously treated Lyme disease. It does not establish that such patients have dementia, nor does it establish a simple relationship between persistent cognitive symptoms and ongoing infection.

In my clinical practice, I have also seen patients with persistent cognitive symptoms after previously treated Lyme disease improve with additional individualized treatment. Others have improved only partially or not at all. This variability is one reason persistent cognitive symptoms require a broader clinical assessment rather than assuming either that every symptom represents active infection or that further improvement is impossible.

Is a Spinal Tap Always Necessary?

No. The role of cerebrospinal fluid testing depends on the clinical presentation and the diagnostic question.

CSF evaluation can be particularly useful when clinicians suspect central nervous system Lyme neuroborreliosis, meningitis, encephalitis, or another inflammatory or infectious neurologic process. Findings may include pleocytosis, elevated protein, and evidence of intrathecal antibody production.

In the best-documented cases of secondary dementia associated with Lyme neuroborreliosis, inflammatory CSF abnormalities helped distinguish the syndrome from primary neurodegenerative dementia.⁴

However, patients presenting primarily with chronic brain fog or cognitive complaints represent a different diagnostic problem from patients with an acute or progressive meningitis, encephalitis, or meningoencephalomyelitis syndrome.

Logigian and colleagues described 27 patients with chronic neurologic manifestations of Lyme disease. Twenty-four had a mild encephalopathy characterized by memory loss, mood changes, or sleep disturbance, while 18 of those 24 had elevated CSF protein, intrathecal antibody production, or both.¹

The study demonstrates that Lyme disease can be associated with chronic neurologic and cognitive abnormalities, but its findings should not be used to conclude that a normal spinal tap universally excludes or confirms neurologic Lyme disease.

The decision to perform lumbar puncture should therefore be individualized according to the neurologic presentation and differential diagnosis.

A Famous Example: Kris Kristofferson

The country music legend Kris Kristofferson was publicly reported to have experienced memory problems that had been attributed to Alzheimer’s disease before Lyme disease was identified as a possible explanation.

His story brought national attention to the broader clinical issue: cognitive symptoms should not automatically be assumed to represent irreversible neurodegenerative disease when the clinical course suggests that another explanation may be present.

A celebrity report cannot establish a medical diagnosis or prove causation. It does, however, illustrate why patients with atypical cognitive decline may warrant a broader diagnostic evaluation.

Why a Careful Evaluation Matters

Cognitive decline has many potential causes. Some are neurodegenerative, while others may be treatable or partially reversible.

Other conditions clinicians may consider include:

• Medication effects
• Thyroid disorders
• Vitamin deficiencies
• Sleep apnea
• Depression and other psychiatric conditions
• Vascular disease
• Normal pressure hydrocephalus
• Autoimmune or inflammatory disorders
• Other neurologic diseases
• Other infections

The 2025 guideline emphasizes a structured evaluation for potentially treatable contributors to cognitive impairment rather than assuming that every dementia-like presentation represents irreversible neurodegeneration.⁷

Lyme disease is one consideration within that broader differential diagnosis—not an explanation for every patient with memory loss.

When Should Lyme Disease Be Considered?

When patients present with new or unexplained cognitive symptoms, Lyme disease may deserve consideration when the clinical history supports it.

• Ask about possible tick exposure, outdoor activities, prior rashes, neurologic symptoms, and residence or travel in endemic areas.
• Look for other neurologic or systemic features that may accompany the cognitive symptoms.
• Consider the tempo of cognitive decline. Rapid or atypical progression may warrant evaluation for secondary causes.
• Interpret Lyme testing in the context of the clinical presentation rather than in isolation.
• Evaluate for other potentially treatable causes of cognitive decline.
• Consider CSF analysis when the neurologic presentation suggests central nervous system Lyme neuroborreliosis or another condition for which spinal fluid evaluation may be informative.
• Continue evaluating for primary neurodegenerative disease when the clinical pattern supports it.

This approach does not mean every patient with dementia has Lyme disease. It means that potentially treatable causes should not be overlooked when cognitive decline is atypical or accompanied by clues pointing toward another diagnosis.

Frequently Asked Questions

Can Lyme disease be mistaken for dementia?

Yes. Lyme disease can sometimes produce brain fog, memory problems, confusion, slowed thinking, and other cognitive symptoms that resemble dementia. Dementia-like syndromes due to Lyme neuroborreliosis have been reported but appear to be uncommon.

Can Lyme disease cause dementia-like symptoms?

Yes. Lyme neuroborreliosis can rarely produce cognitive syndromes that resemble dementia. Lyme disease is not, however, an established cause of Alzheimer’s disease or other primary neurodegenerative dementias.

Does Lyme disease cause Alzheimer’s disease?

Lyme disease has not been established as a cause of Alzheimer’s disease. Researchers are investigating whether microbes, including Borrelia burgdorferi, might influence inflammatory, amyloid, tau, or other biological pathways involved in Alzheimer’s disease, but this research does not demonstrate that Lyme disease causes Alzheimer’s disease.

Does Lyme disease increase the risk of dementia?

Current population evidence does not demonstrate an increased long-term risk of dementia or Alzheimer’s disease following Lyme neuroborreliosis. This is different from the rare dementia-like cognitive syndromes that have been reported during neurologic Lyme disease.

Can Lyme disease cause memory loss?

Yes. Cognitive symptoms associated with Lyme disease may include short-term memory problems, forgetfulness, difficulty concentrating, slowed processing, and word-finding difficulty.

Can Lyme disease be mistaken for Alzheimer’s disease?

It can occasionally resemble Alzheimer’s disease when cognitive symptoms dominate the presentation. Rapid or atypical progression, other neurologic or systemic symptoms, and plausible tick exposure may prompt clinicians to consider alternative diagnoses. Lyme disease has not been established as a cause of Alzheimer’s disease.

Is Lyme-related cognitive decline reversible?

Some reported patients with Lyme neuroborreliosis and dementia-like cognitive impairment have improved after appropriate treatment. However, improvement is not guaranteed, and potentially treatable cognitive impairment should not be equated with completely reversible dementia.

Should everyone with dementia be tested for Lyme disease?

No. Lyme testing is most appropriate when symptoms, exposure history, geographic risk, neurologic findings, or other features raise reasonable clinical suspicion. A positive antibody test alone does not establish that Lyme disease is causing dementia.

Does a normal spinal tap rule out every form of neurologic Lyme disease?

CSF testing is particularly useful when central nervous system Lyme neuroborreliosis is suspected, but its interpretation depends on the clinical syndrome and the diagnostic criteria being applied. A spinal tap should be considered as one part of a broader neurologic evaluation rather than as a stand-alone answer to chronic cognitive symptoms.

What is the difference between Lyme brain fog and dementia?

Lyme-related brain fog often involves difficulty concentrating, slowed thinking, word retrieval, mental stamina, and short-term memory. Dementia involves cognitive decline severe enough to interfere with independent daily functioning and may result from Alzheimer’s disease or many other conditions.

Clinical Takeaway

Lyme disease can sometimes produce cognitive symptoms that resemble dementia, but dementia-like Lyme neuroborreliosis appears to be uncommon and Lyme disease is not an established cause of Alzheimer’s disease.

The most useful distinction is between a secondary dementia-like neurologic syndrome and a primary neurodegenerative dementia. Published cases demonstrate that Lyme neuroborreliosis can occasionally produce substantial cognitive decline and that some patients improve after antibiotic treatment.^2-5

At the same time, population data have not shown an increased long-term risk of dementia or Alzheimer’s disease following Lyme neuroborreliosis, and reviews have not established Lyme disease as a cause of Alzheimer’s disease or Lewy body dementia.^8,9

The 2025 clinical practice guideline adds an important contemporary point: Lyme disease remains among the neuroinfectious conditions clinicians may consider when investigating potentially treatable causes of cognitive impairment.⁷

The practical message is not that dementia should routinely be attributed to Lyme disease. It is that when cognitive decline is atypical, rapidly progressive, fluctuating, or accompanied by other neurologic or systemic clues, potentially treatable causes—including Lyme disease in the appropriate clinical setting—should not be overlooked.

Related Articles

These related articles explore cognitive symptoms, neurologic Lyme disease, misdiagnosis, and potentially reversible dementia-like presentations.

• Lyme Disease Brain Fog: Causes, Symptoms, and Treatment
• Neurologic Lyme Disease Symptoms: How Lyme Affects the Nervous System
• Lyme Disease Misdiagnosis: Why It Happens and What to Know
• Lyme Disease Symptoms: Why They Come and Go
• Can Lyme Disease Mimic Dementia? When Cognitive Decline May Be Reversible

References

1. Logigian EL, Kaplan RF, Steere AC. Chronic neurologic manifestations of Lyme disease. N Engl J Med. 1990;323(21):1438-1444. doi:10.1056/NEJM199011223232102. PMID: 2172819.
2. Blanc F, Philippi N, Cretin B, et al. Lyme neuroborreliosis and dementia. J Alzheimers Dis. 2014;41(4):1087-1093. doi:10.3233/JAD-130446. PMID: 24762944.
3. Sanchini C, Papia C, Cutaia C, Poloni TE, Cesari M. A Case of Reversible Dementia? Dementia vs Delirium in Lyme Disease. Ann Geriatr Med Res. 2023;27(1):80-82. doi:10.4235/agmr.22.0128. PMID: 36740841; PMCID: PMC10073979.
4. Kristoferitsch W, Aboulenein-Djamshidian F, Jecel J, et al. Secondary dementia due to Lyme neuroborreliosis. Wien Klin Wochenschr. 2018;130(15-16):468-478. doi:10.1007/s00508-018-1361-9. PMID: 30046879.
5. Bashchobanov DH, Stamatova E, Andonova R, et al. Lyme Neuroborreliosis in the Context of Dementia Syndromes. Cureus. 2024;16(8):e67057. doi:10.7759/cureus.67057. PMCID: PMC11403646.
6. Fallon BA, Keilp JG, Corbera KM, et al. A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy. Neurology. 2008;70(13):992-1003. doi:10.1212/01.WNL.0000284604.61160.2d. PMID: 17928580.
7. Siddiqui MA, Garg S, Tikka SK. Clinical practice guidelines on addressing cognitive impairment in treatable dementias. Indian J Psychiatry. 2025;67(1):41-53. doi:10.4103/indianjpsychiatry.indianjpsychiatry_684_24. PMID: 40046486; PMCID: PMC11878466.
8. Wormser GP, Marques A, Pavia CS, Schwartz I, Feder HM Jr, Pachner AR. Lack of Convincing Evidence That Borrelia burgdorferi Infection Causes Either Alzheimer Disease or Lewy Body Dementia. Clin Infect Dis. 2022;75(2):342-346. doi:10.1093/cid/ciab993. PMID: 34849631; PMCID: PMC9410724.
9. Haahr R, Tetens MM, Dessau RB, et al. Risk of Neurological Disorders in Patients With European Lyme Neuroborreliosis: A Nationwide, Population-Based Cohort Study. Clin Infect Dis. 2020;71(6):1511-1516. doi:10.1093/cid/ciz997. PMID: 31598647.
10. Williams ZAP, Lang L, Nicolas S, et al. Do microbes play a role in Alzheimer’s disease? Microb Biotechnol. 2024;17(4):e14462. doi:10.1111/1751-7915.14462. PMID: 38593310; PMCID: PMC11003713.

This article is for informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment.

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Dr. Daniel Cameron, MD, MPH
Lyme disease clinician with over 30 years of experience and past president of ILADS.

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