Can Human Cytomegalovirus Infections Spark Alzheimer’s Pathology?

A growing body of work implicates infections as a risk factor for Alzheimer’s disease. In the December 19 Alzheimer’s & Dementia, scientists led by Benjamin Readhead at Arizona State University, Tempe, and Eric Reiman at Banner Alzheimer’s Institute, Phoenix, add the latest evidence. In postmortem tissue from AD patients, they found that those who had a particular type of activated microglia in the brain also had human cytomegalovirus infections in the brain, vagal nerve, and gut. In human cerebral organoids, HCMV promoted Aβ and p-tau212 accumulation, suggesting that these infections could kick off AD pathology in the brain. “We think the virus contributes to AD,” Readhead told Alzforum.

  • Almost half of AD patients examined had HCMV infections in the brain and gut.
  • These patients also produced IgG4 and had CD83+ microglia in the brain.
  • HCMV promoted amyloid and tau pathology in cerebral organoids, suggesting a potential causal role.

Brian Balin at the Philadelphia College of Osteopathic Medicine agreed. “Infections may be the early upstream drivers of disease, and we need to focus on how to more precisely diagnosis what may be onboard prior to disease onset and to intervene, if possible, with appropriate drug regimens,” he wrote to Alzforum (comment below). Balin participates in the Alzheimer’s Pathobiome Initiative, which investigates whether treatment with antimicrobials can prevent or slow AD.

HCMV in AD. People who had CD83+ microglia (red) in the prefrontal cortex also had human cytomegalovirus (green), both clustered around dense core plaques. Nuclei are blue. [Courtesy of Readhead et al., Alzheimer’s & Dementia.]

Readhead and colleagues did not set out to study infections. Previously, they had performed single-nuclei RNA-Seq on postmortem superior frontal gyri from 66 AD patients and 35 controls to characterize cellular changes. In 31 AD patients and nine controls, they found a microglial subtype marked by expression of CD83. This receptor is found on antigen-presenting cells and regulates their immune responses. These CD83+ microglia also expressed genes related to antibody and complement responses, lipid and iron processing, and senescence. Their presence in AD brains correlated with a higher burden of plaques and tangles (Wang et al., 2024). 

In the present paper, the authors followed up. Because immune dendritic cells express CD83 when fighting pathogens, first author Readhead searched for signs of infection in tissue from donors who had CD83+ microglia. The donors participated in the Banner Sun Health Research Institute Brain and Body Donation Program, hence multiple types of tissue from the same individuals were available (Beach et al., 2015). The authors first examined the transverse colon, a hotbed of immune activity in the body. For that, they had tissue from nine AD patients with CD83+ microglia in the brain, and from five AD patients without these microglia.

In all nine samples from the CD83+ group, and one from the CD83- group, the authors detected active HCMV infections (image below). HCMV is a ubiquitous virus found in nearly all adults, but in most, it remains dormant. The presence of HCMV immunoreactivity in the gut suggests a failure of the peripheral immune system to suppress this virus, Readhead told Alzforum. He is trying to figure out why this happens.

In this study, it turned out that HCMV had not stayed in the gut. In every donor from the CD83+ group, the virus had also invaded the vagal nerve and the superior frontal gyrus. This implies it may travel through the vagal nerve to reach the brain, a route implicated in the pathogen theory of Parkinson’s disease (Dec 2016 news; Jul 2019 conference news; Sep 2024 news).

Gut-Brain Connection. People who have CD83+ microglia in their brains also have HCMV (top left) and IgG4 (top right) in their guts. People without CD83+ microglia (bottom) do not. [Courtesy of Readhead et al., Alzheimer’s & Dementia.]

The CD83+ group also produced IgG4 antibodies, many of which recognized HCMV antigens. These antibodies were present in transverse colon, vagal nerve, brain, and cerebrospinal fluid. IgG4 antibodies are rare under normal circumstances. They have an anti-inflammatory effect, binding antigens without triggering phagocytosis or complement activation, and usually serve to quiet allergic reactions.

Why do they occur in HCMV infections? Readhead suggested two possibilities: either the body activates them in chronic infections to tamp down its immune response and avoid collateral tissue damage, or the virus itself spurs their production, perhaps to confuse host immune responses. The authors are now investigating whether IgG4 in the blood could be used as a biomarker of HCMV infections.

The authors replicated their findings in an independent cohort from the Religious Orders Study and Rush Memory and Aging Project. In postmortem prefrontal cortex samples from AD patients, 10 of 13 that had CD83+ microglia also had HCMV, while three of 14 without these microglia did. The authors infected cultured human microglia with HCMV and confirmed that the virus promoted CD83+ expression. Herpes virus and lipopolysaccharide did not, suggesting that CD83+ is specific for HCMV.

What might HCMV do to the brain? To approach this, the authors turned to human cerebral organoids. Infecting them with HCMV revved up Aβ42 and p-tau212 production, as well as neuron death. The amount of Aβ and tau strongly correlated with the abundance of HCMV in the dead neurons, with a coefficient of around r=0.7. In live organoid neurons, that coefficient was 0.3. Intriguingly, one prior study linked HCMV infection to a lower plasma Aβ42/40 ratio, hinting that the virus might promote amyloidosis (Parker et al., 2024).

Jacob Raber at Oregon Health and Science University, Portland, agreed these data support the idea that HCMV infection contributes to AD. He believes they also highlight the importance of the gut-brain axis in the disease. Raber noted that a previous study reported changes in the gut microbiome in people with preclinical AD compared with healthy controls (Ferreiro et al., 2023). “Increased efforts are warranted to better understand the role of (re)activation of neurotropic viruses and associated inflammation and AD pathology in the gut,” he wrote to Alzforum (comment below).

Why have some previous studies reported no increased risk of AD in people positive for HCMV (Vestin et al., 2024; Ma et al., 2024)? Those tested for HCMV immunoreactivity in the blood, a form of testing that does not distinguish between dormant and active infections. Readhead believes only people with an active HCMV infection in the gut are at elevated risk. If a biomarker for this can be developed, Readhead and colleagues will test whether antivirals can slow or prevent symptoms in people who are positive for active HCMV and AD biomarkers.

Herpes virus has been linked to AD as well (Jun 2018 news; Feb 2021 news; Apr 2021 conference news). A Phase 2 trial of the antiviral valacyclovir in people with mild AD and herpes infections is ongoing at Columbia University, and was expected to complete at the end of 2024 (Devanand, 2018).

Other work has implicated viral infections in general, including influenza, with an increased risk for several neurodegenerative diseases (Feb 2023 news). It seems likely this research area will only heat up in the years to come.—Madolyn Bowman Rogers

Comments

    • User Profile Image Brian Balin
      Philadelphia College of Osteopathic Medicine
    • Posted:

    This article provides an intriguing insight into infection with human cytomegalovirus and its connection with Alzheimer’s disease. The work further supports an infectious process that can result in specific changes in the brain and relevant cell types consistent with the pathogenesis process of AD (Itzhaki et al., 2016). Involvement of the gut and brain changes and infectivity in both areas highlights features of the gut-brain axis that may be important for general consideration in infection-related neurodegenerative conditions.

    While this report focuses on one infectious agent involved in disease, many of us, as part of the Alzheimer’s Pathobiome Initiative, have been studying infection in AD for decades (Lathe et al., 2023; Bathini et al., 2024), and realize that we need to consider a polymicrobial approach to understanding the wide-ranging relationships of infections with AD as well as the many other neurodegenerative diseases. These findings are very important in the sense that infections may be early upstream drivers of disease. We need to focus on how to more precisely diagnose what may be onboard prior to disease onset, and to intervene, if possible, with appropriate drug regimens. In this regard, there are notable cases of “reversible dementias” for which an infectious agent was determined to be present, followed by precise therapeutic interventions to effectively treat (Lathe et al., 2023). 

    Intriguingly, the findings of HCMV associated with CD83+ microglia in the superior frontal cortex but not reported for other brain regions leads one to consider that different brain regions and cells therein may be insulted with different microbial organisms with varying degrees of virulence. Furthermore, the routes of infections into the brain need to be considered in regard to the different organisms that have been associated with AD and other neurological conditions. For example, respiratory organisms may use the olfactory system for uptake and further brain involvement, whereas those infecting other sensory systems such as vision and hearing could use other cranial nerve involvement, much like gut organisms using the vagal nerve for potential uptake (Bathini et al., 2024).

    Other important considerations with regard to infections as drivers of AD pathogenesis are selective vulnerability in brain regions and genetic predisposition. As a number of the neurodegenerative conditions appear to start in discrete brain regions, a consideration of structure to function relationships can provide clues as to where an infectious insult may be principally important. Genetic predispositions may include those such as the APOE genotype and HLA expression.

    The overall message from studies such as this is that we need to study the relationships between infection (often chronic, persistent, latent) within the nervous system and neurological insult, because they go well beyond our recognition of the typical designations of meningitis, encephalitis, meningoencephalitis.   

    References:

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    Lathe R, Schultek NM, Balin BJ, Ehrlich GD, Auber LA, Perry G, Breitschwerdt EB, Corry DB, Doty RL, Rissman RA, Nara PL, Itzhaki R, Eimer WA, Tanzi RE, Intracell Research Group Consortium Collaborators. Establishment of a consensus protocol to explore the brain pathobiome in patients with mild cognitive impairment and Alzheimer's disease: Research outline and call for collaboration. Alzheimers Dement. 2023 Nov;19(11):5209-5231. Epub 2023 Jun 7 PubMed.

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    View all comments by Brian Balin

  2. In this original and timely study, Readhead et al. followed up on their earlier data showing that an AD-related CD83(+) microglia subtype associated with increased immunoglobulinG4 (IgG4) in the transverse colon (Wang et al., 2024). In the current study, CD83(+) microglia in the superior frontal gyrus were associated with elevated levels of IgG4 and human cytomegalovirus in the TC, anti-HCMV IgG4 in CSF, and HCMV and IgG4 in the SFG and vagal nerve. In addition, HCMV-infected cerebral organoids showed enhanced AD pathology, namely Aβ42 and pTau-212, and neuronal death. The CD83(+) microglia might not be specific to AD, as they were also noted in the EAE multiple sclerosis model (Sinner et al., 2023). The association between viruses and AD is not limited to HCMV and has been proposed for reactivated Herpes Simplex (Itzhaki, 1994) and other neurotropic viruses as well; the viral association is not limited to AD, either, but has been made with other neurodegenerative conditions (Levine et al., 2023). 

    While HCMV is very common in the blood in the elderly, HCMV in the TC is not (Chen et al., 2021). HCMV in the TC is associated with CD83(+) microglia and HCMV in the SFG, supporting key roles for the gut microbiome and gut-liver-brain axis in AD. Consistent with such roles, Ferreiro et al. reported that in cognitively healthy 68- to 94-year -olds, there are gut-microbiome correlates of preclinical AD neuropathology (Aβ and tau biomarkers), and that inclusion of microbiome features that associated with preclinical AD improved prediction of preclinical AD status (Ferreiro et al., 2023). In addition, the human gut microbiome diversifies with age, reflects healthy vs. unhealthy aging, associates with a healthy lipid profile, and predicts survival (Wilmanski et al., 2021), while alterations in microbiome composition have been linked to AD and impact AD-associated behaviors and brain pathologies (Kundu et al., 2022; Kundu et al., 2021; Marizzoni et al., 2020).

    That HCMV-infected cerebral organoids enhance Aβ42 and p-tau212 supports a causal role of viral infection in AD pathology. As the gut-liver-brain axis is bi-directional, it is not clear yet whether, in the case of HCMV, viral replication and/or reactivation is originally or mainly driven by the gut and/or brain. Regardless, given other studies supporting the role of the gut microbiome in AD mouse models (Kundu et al., 2021), AD, and Parkinson’s disease (Santos et al., 2019; Elfil et al., 2020; Keshvarzian et al., 2020; Koutzoumis et al., 2020; Sampson et al., 2016; Torres et al., 2018), increased efforts are warranted to better understand the role of (re)activation of neurotropic viruses and associated inflammation and AD pathology in the gut, and whether antivirals and/or other microbiome-targeted strategies can delay or even prevent incidence or severity of AD.

    References:

    Chen S, Pawelec G, Trompet S, Goldeck D, Mortensen LH, Slagboom PE, Christensen K, Gussekloo J, Kearney P, Buckley BM, Ford I, Jukema JW, Westendorp RG, Maier AB. Associations of Cytomegalovirus Infection With All-Cause and Cardiovascular Mortality in Multiple Observational Cohort Studies of Older Adults. J Infect Dis. 2021 Feb 3;223(2):238-246. PubMed.

    Elfil M, Kamel S, Kandil M, Koo BB, Schaefer SM. Implications of the Gut Microbiome in Parkinson's Disease. Mov Disord. 2020 Jun;35(6):921-933. Epub 2020 Feb 24 PubMed.

    Ferreiro AL, Choi J, Ryou J, Newcomer EP, Thompson R, Bollinger RM, Hall-Moore C, Ndao IM, Sax L, Benzinger TL, Stark SL, Holtzman DM, Fagan AM, Schindler SE, Cruchaga C, Butt OH, Morris JC, Tarr PI, Ances BM, Dantas G. Gut microbiome composition may be an indicator of preclinical Alzheimer's disease. Sci Transl Med. 2023 Jun 14;15(700):eabo2984. PubMed.

    Santos SF, de Oliveira HL, Yamada ES, Neves BC, Pereira A Jr. The Gut and Parkinson's Disease-A Bidirectional Pathway. Front Neurol. 2019;10:574. Epub 2019 Jun 4 PubMed.

    Itzhaki RF. Possible factors in the etiology of Alzheimer's disease. Mol Neurobiol. 1994 Aug-Dec;9(1-3):1-13. PubMed.

    Keshavarzian A, Engen P, Bonvegna S, Cilia R. The gut microbiome in Parkinson's disease: A culprit or a bystander?. Prog Brain Res. 2020;252:357-450. Epub 2020 Mar 5 PubMed.

    Koutzoumis DN, Vergara M, Pino J, Buddendorff J, Khoshbouei H, Mandel RJ, Torres GE. Alterations of the gut microbiota with antibiotics protects dopamine neuron loss and improve motor deficits in a pharmacological rodent model of Parkinson's disease. Exp Neurol. 2020 Mar;325:113159. Epub 2019 Dec 13 PubMed.

    Kundu P, Stagaman K, Kasschau K, Holden S, Shulzhenko N, Sharpton TJ, Raber J. Fecal Implants From App NL-G-F and App NL-G-F/E4 Donor Mice Sufficient to Induce Behavioral Phenotypes in Germ-Free Mice. Front Behav Neurosci. 2022;16:791128. Epub 2022 Feb 8 PubMed.

    Kundu P, Torres ER, Stagaman K, Kasschau K, Okhovat M, Holden S, Ward S, Nevonen KA, Davis BA, Saito T, Saido TC, Carbone L, Sharpton TJ, Raber J. Integrated analysis of behavioral, epigenetic, and gut microbiome analyses in AppNL-G-F, AppNL-F, and wild type mice. Sci Rep. 2021 Feb 25;11(1):4678. PubMed.

    Levine KS, Leonard HL, Blauwendraat C, Iwaki H, Johnson N, Bandres-Ciga S, Ferrucci L, Faghri F, Singleton AB, Nalls MA. Virus exposure and neurodegenerative disease risk across national biobanks. Neuron. 2023 Apr 5;111(7):1086-1093.e2. Epub 2023 Jan 19 PubMed.

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    Sinner P, Peckert-Maier K, Mohammadian H, Kuhnt C, Draßner C, Panagiotakopoulou V, Rauber S, Linnerbauer M, Haimon Z, Royzman D, Kronenberg-Versteeg D, Ramming A, Steinkasserer A, Wild AB. Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune encephalomyelitis. Nat Commun. 2023 Aug 1;14(1):4601. PubMed.

    Torres ER, Akinyeke T, Stagaman K, Duvoisin RM, Meshul CK, Sharpton TJ, Raber J. Effects of Sub-Chronic MPTP Exposure on Behavioral and Cognitive Performance and the Microbiome of Wild-Type and mGlu8 Knockout Female and Male Mice. Front Behav Neurosci. 2018;12:140. Epub 2018 Jul 18 PubMed.

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  3. The growing body of literature linking herpesviruses to neurodegenerative processes has evolved from observational cohort studies to mechanistic experimental research. Observational studies have shown that antiherpetic drugs are associated with a reduced risk of developing neurodegenerative dementias such as Alzheimer's disease. Experimental models have provided complementary evidence, with herpes simplex virus 1 (HSV-1) shown to induce Aβ aggregation in vitro and in vivo. Readhead et al.’s findings extend this research by implicating human cytomegalovirus in AD pathology through cross-tissue immunological mechanisms involving CD83(+) microglia and immunoglobulin G4 (IgG4) responses. This study's integration of histological, immunological, and transcriptomic data reinforces the infectious hypothesis in AD, supporting a more comprehensive, mechanistically driven model of herpesvirus-induced neurodegeneration.

    Herpesviridae are widespread in the human population, yet only a subset of individuals experience viral reactivation and increased neurodegenerative risk. While immunosuppression is a well-recognized trigger, as seen in shingles outbreaks among immunocompromised individuals, the exact mechanism remains unclear. Reactivation may be influenced by viral latency reservoirs, chronic inflammation, and cellular senescence. Readhead et al. propose that HCMV persistence in gut tissues could enable periodic reactivation, facilitated by immunosenescence or gut-brain axis dysfunction. However, broader investigations into viral strain variations, host immune-genetic factors, and co-infections are warranted. Indeed, pathogenic symbiosis of HCMV with HSV-1 (Lövheim et al., 2018) or EBV (Torniainen-Holm et al., 2018) has been previously reported and other pathobiont species have been implicated besides Human Herpesviridae (Zilli et al., 2021). In practical terms, the investigation of polymicrobial infections (bacterial, viral and fungal) is multidimensional, requiring a multipronged effort, such as the one from the Alzheimer’s Pathobiome Initiative, a research consortium committed to unravel and translate the infectious etiology of AD.

    Nevertheless, the study highlights HCMV as the primary viral agent inducing AD-like neuropathology in cerebral organoids, while noting that lipopolysaccharide (LPS) and human herpesvirus 6A (HHV-6A) failed to produce similar effects. This contrasts with prior research where LPS-induced AD-like pathology (Zhan et al., 2018) while HHV-6A’s subtler contributions to neuroinflammation are documented. This discrepancy might be attributable to the specific cellular composition of the organoid models used or to differences in viral titers and infection protocols. Expanding to more diverse in vitro models could clarify these differential responses.

    The study proposes a gut-brain axis mediated by the vagus nerve as a plausible gateway for HCMV entry into the brain, supported by histological evidence of viral presence along this route. This explanation may be incomplete. HCMV is known to establish latency in hematopoietic progenitor cells and endothelial tissues, suggesting that alternative routes such as hematogenous dissemination through infected monocytes could also play a role, particularly in conditions of endothelial permeability and vascular damage. Future work should consider multi-organ viral dynamics to build a more comprehensive model of central nervous system (CNS) invasion.

    An important contribution of this study is the identification of HCMV-specific IgG4 antibodies, implicating a potential viral immune evasion strategy. IgG4’s known anti-inflammatory properties may facilitate chronic viral persistence by dampening host immune responses. Understanding how IgG4-driven immune suppression influences both viral reactivation and neurodegeneration could open new therapeutic avenues, including immunomodulatory treatments targeting the adaptive immune system.

    These findings add to the increasing and highly debated literature implicating microbial infections in Alzheimer’s disease (AD) etiology. From Ruth Itzhaki’s pioneering work linking HSV-1 to AD pathology (Itzhaki et al., 1997; Itzhaki, 2021), 30 years of research have explored microbial neurotropism, particularly Herpesviridae. Observational studies showed antiherpetic drugs reduce dementia risk (Tzeng et al., 2018; Lövheim et al., 2019; Schnier et al., 2021), but enthusiasm for these treatments has been lukewarm due to skepticism about causality. Recent experimental evidence—such as HSV-1’s ability to induce Aβ aggregation as an antimicrobial trap—has shifted the conversation toward antiviral interventions (Eimer et al., 2018). However, funding challenges persist, limiting deeper exploration of microbial or polymicrobial triggers.

    Readhead et al.’s untargeted search for HCMV reactivity in AD brains represents a less-biased approach that aligns with prior studies often dismissed as exotic. Herpesviridae’s ubiquity complicates public health implications, as reactivation risks remain poorly understood. Addressing reactivation mechanisms requires personalized approaches that may be resource-intensive. Nevertheless, vaccines like BCG (against M. tuberculosis) (Weinberg et al., 2023) or Shingrix (against VZV)—shown to reduce inflammation and viral reactivation—could prevent cascades leading to neurodegeneration, including chronic inflammation and blood-brain barrier permeability.

    The possibility that microbial reactivation occurs decades before cognitive symptoms underscores the need for early intervention. Precision medicine using artificial intelligence to identify individual risk trajectories could redefine preventive strategies. Bold investment in alternative therapeutic mechanisms, including infection-focused approaches, is crucial for advancing AD treatment paradigms.

    References:

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    Tzeng NS, Chung CH, Lin FH, Chiang CP, Yeh CB, Huang SY, Lu RB, Chang HA, Kao YC, Yeh HW, Chiang WS, Chou YC, Tsao CH, Wu YF, Chien WC. Anti-herpetic Medications and Reduced Risk of Dementia in Patients with Herpes Simplex Virus Infections-a Nationwide, Population-Based Cohort Study in Taiwan. Neurotherapeutics. 2018 Apr;15(2):417-429. PubMed.

    Lövheim H, Norman T, Weidung B, Olsson J, Josefsson M, Adolfsson R, Nyberg L, Elgh F. Herpes Simplex Virus, APOEɛ4, and Cognitive Decline in Old Age: Results from the Betula Cohort Study. J Alzheimers Dis. 2019;67(1):211-220. PubMed.

    Schnier C, Janbek J, Williams L, Wilkinson T, Laursen TM, Waldemar G, Richter H, Kostev K, Lathe R, G Haas J. Antiherpetic medication and incident dementia: Observational cohort studies in four countries. Eur J Neurol. 2021 Jun;28(6):1840-1848. Epub 2021 Mar 19 PubMed.

    Eimer WA, Vijaya Kumar DK, Navalpur Shanmugam NK, Rodriguez AS, Mitchell T, Washicosky KJ, György B, Breakefield XO, Tanzi RE, Moir RD. Alzheimer's Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection. Neuron. 2018 Jul 11;99(1):56-63.e3. PubMed.

    Weinberg MS, Zafar A, Magdamo C, Chung SY, Chou WH, Nayan M, Deodhar M, Frendl DM, Feldman AS, Faustman DL, Arnold SE, Vakulenko-Lagun B, Das S. Association of BCG Vaccine Treatment With Death and Dementia in Patients With Non-Muscle-Invasive Bladder Cancer. JAMA Netw Open. 2023 May 1;6(5):e2314336. PubMed.

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References

News Citations

  1. Do Microbes in the Gut Trigger Parkinson’s Disease?
  2. In PD Model, α-Synuclein Spreads from Intestine to Brain
  3. Damage to the Gut Mucosa May Almost Double Parkinson's Risk
  4. Herpes Triggers Amyloid—Could This Virus Fuel Alzheimer’s?
  5. Herpes Update—Virus Increases Dementia Risk in Sweden
  6. More Data on Herpes and Alzheimer’s Disease
  7. Nothing to Sneeze At: Viruses Raise Risk of Neurodegenerative Disease

Therapeutics Citations

  1. Valacyclovir

Paper Citations

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  4. Ferreiro AL, Choi J, Ryou J, Newcomer EP, Thompson R, Bollinger RM, Hall-Moore C, Ndao IM, Sax L, Benzinger TL, Stark SL, Holtzman DM, Fagan AM, Schindler SE, Cruchaga C, Butt OH, Morris JC, Tarr PI, Ances BM, Dantas G. Gut microbiome composition may be an indicator of preclinical Alzheimer's disease. Sci Transl Med. 2023 Jun 14;15(700):eabo2984. PubMed.
  5. Vestin E, Boström G, Olsson J, Elgh F, Lind L, Kilander L, Lövheim H, Weidung B. Herpes Simplex Viral Infection Doubles the Risk of Dementia in a Contemporary Cohort of Older Adults: A Prospective Study. J Alzheimers Dis. 2024;97(4):1841-1850. PubMed.
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External Citations

  1. Alzheimer’s Pathobiome Initiative

Further Reading

Primary Papers

  1. Readhead BP, Mastroeni DF, Wang Q, Sierra MA, de Ávila C, Jimoh TO, Haure-Mirande JV, Atanasoff KE, Nolz J, Suazo C, Barton NJ, Orszulak AR, Chigas SM, Tran K, Mirza A, Ryon K, Proszynski J, Najjar D, Dudley JT, Liu ST, Gandy S, Ehrlich ME, Alsop E, Antone J, Reiman R, Funk C, Best RL, Jhatro M, Kamath K, Shon J, Kowalik TF, Bennett DA, Liang WS, Serrano GE, Beach TG, Van Keuren-Jensen K, Mason CE, Chan Y, Lim ET, Tortorella D, Reiman EM. Alzheimer's disease-associated CD83(+) microglia are linked with increased immunoglobulin G4 and human cytomegalovirus in the gut, vagal nerve, and brain. Alzheimers Dement. 2024 Dec 19; Epub 2024 Dec 19 PubMed.

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