The impact of peptic ulcer disease (PUD) and Helicobacter pylori (H. pylori) eradication therapy on dementia risk in high H. pylori prevalence populations remains uncertain. This study investigates the relationship between PUD, H. pylori eradication, and dementia risk, including Alzheimer's disease (AD), in an elderly South Korean cohort, considering age and eradication timing. Data from the Korean National Health Insurance Service (2002-2015) for individuals aged 55-79 were analyzed. Participants were divided based on PUD and H. pylori therapy status. Propensity score matching was used to evaluate dementia incidence and hazard ratios over 5 and 10 years, alongside the timing of eradication therapy. PUD is linked to higher dementia risk at 5 and 10 years, more for overall dementia than AD, with eradication status not significantly altering the risk. Age-specific analysis showed increased AD risk in the 60s and 70s age groups. Late eradication therapy is correlated with a higher dementia risk. PUD is a risk factor for dementia in elderly South Koreans, particularly with delayed H. pylori therapy. The findings emphasize timely H. pylori management and its potential role in neurodegenerative disease prevention.

Alzheimer's Disease (AD) is the most prevalent type of dementia and is characterized by the presence of senile plaques and neurofibrillary tangles. There are various theories concerning the causes of AD, but the connection between viral and bacterial infections and their potential role in the pathogenesis of AD has become a fascinating area of research for the field. Various viruses such as Herpes simplex virus 1 (HSV-1), Epstein-Barr virus (EBV), Cytomegalovirus (CMV), influenza viruses, and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), as well as bacteria such as Chlamydia pneumoniae (CP), Helicobacter pylori (HP), Porphyromonas gingivalis (P. gingivalis), Spirochetes and eukaryotic unicellular parasites (e.g., Toxoplasma gondii), have been linked to AD due to their ability to activate the immune system, induce inflammation and increase oxidative stress, thereby leading to cognitive decline and AD. In addition, microRNAs (miRNAs) might play a crucial role in the pathogenesis mechanisms of these pathogens since they are utilized to target various protein-coding genes, allowing for immune evasion, maintaining latency, and suppressing cellular signaling molecules. Also, they can regulate gene expression in human cells. This article provides an overview of the association between AD and various infectious agents, with a focus on the mechanisms by which these pathogens may be related to the pathogenesis of AD. These findings suggest important areas for further research to be explored in future studies.

Alzheimer's disease (AD) is a global health concern and the leading cause of dementia in the elderly. The prevalence of this neurodegenerative condition is projected to increase concomitantly with increased life expectancy, resulting in a significant economic burden. With very few FDA-approved disease-modifying drugs available for AD, there is an urgent need to develop new compounds capable of impeding the progression of the disease. Given the unclear etiopathogenesis of AD, this review emphasizes the underlying mechanisms of this condition. It explores not only well-studied aspects, such as the accumulation of Aβ plaques and neurofibrillary tangles, but also novel areas, including glymphatic and lymphatic pathways, microbiota and the gut-brain axis, serotoninergic and autophagy alterations, vascular dysfunction, the metal hypothesis, the olfactory pathway, and oral health. Furthermore, the potential molecular targets arising from all these mechanisms have been reviewed, along with novel promising approaches such as nanoparticle-based therapy, neural stem cell transplantation, vaccines, and CRISPR-Cas9-mediated genome editing techniques. Taking into account the overlap of these various mechanisms, individual and combination therapies emerge as the future direction in the AD strategy.

More than half of the world's population are colonized with H. pylori; however, the prevalence varies geographically with the highest incidence in Africa. H. pylori is probably a commensal organism that has been associated with the development of gastritis, ulcers, and gastric cancer. H. pylori alone is most probably not enough for the development of gastric carcinoma, but evidence for its association with the disease is high and has, therefore, been classified by the International Agency for Research on Cancer as a Class 1 carcinogen. Bacteroidetes and Fusobacteria positively coexisted during H. pylori infection along the oral-gut axis. The eradication therapy required to treat H. pylori infection can also have detrimental consequences for the gut microbiota, leading to a decreased alpha diversity. Therefore, therapy regimens integrated with probiotics may abolish the negative effects of antibiotic therapy on the gut microbiota. These eradication therapies combined with probiotics have also higher rates of eradication, when compared to standard treatments, and are associated with reduced side effects, improving the patient's compliance. The eradication therapy not only affects gut microbiome but also affects the oral microbiome with robust predominance of harmful bacteria. However, there have been reports of a protective role of H. pylori in Barrett's esophagus, esophageal adenocarcinoma, eosinophilic esophagitis, IBD, asthma, and even multiple sclerosis. Therefore, eradication therapy should be carefully considered, and test to treat policy should be tailored to specific communities especially in highly endemic areas. Supplementation of probiotics, prebiotics, herbals, and microbial metabolites to reduce the negative effects of eradication therapy should be considered. After failure of many eradication attempts, the benefits of H. pylori eradication should be carefully balanced against the risk of adverse effects especially in the elderly, persons with frailty, and intolerance to antibiotics.

Alzheimer's disease (AD) is the primary cause of dementia and is characterized by the death of brain cells due to the accumulation of insoluble amyloid plaques, hyperphosphorylation of tau protein, and the formation of neurofibrillary tangles within the cells. AD is also associated with other pathologies such as neuroinflammation, dysfunction of synaptic connections and circuits, disorders in mitochondrial function and energy production, epigenetic changes, and abnormalities in the vascular system. Despite extensive research conducted over the last hundred years, little is established about what causes AD or how to effectively treat it. Given the severity of the disease and the increasing number of affected individuals, there is a critical need to discover effective medications for AD. The US Food and Drug Administration (FDA) has approved several new drug molecules for AD management since 2003, but these drugs only provide temporary relief of symptoms and do not address the underlying causes of the disease. Currently, available medications focus on correcting the neurotransmitter disruption observed in AD, including cholinesterase inhibitors and an antagonist of the N-methyl-D-aspartate (NMDA) receptor, which temporarily alleviates the signs of dementia but does not prevent or reverse the course of AD. Research towards disease-modifying AD treatments is currently underway, including gene therapy, lipid nanoparticles, and dendrimer-based therapy. These innovative approaches aim to target the underlying pathological processes of AD rather than just managing the symptoms. This review discusses the novel aspects of pathogenesis involved in the causation of AD of AD and in recent developments in the therapeutic armamentarium for the treatment of AD such as gene therapy, lipid nanoparticles, and dendrimer-based therapy, and many more.

Associated with gastritis, peptic-ulcer disease, and gastric carcinoma, Helicobacter pylori (H. pylori) also has been associated with decreased cognitive function and dementia. In this study, we used data from the UK Biobank to further examine associations between H. pylori seropositivity and serointensity and performance on several cognitive tasks in adults 40 to 70 years of age (M = 55.3, SD = 8.1). In these analyses, H. pylori seropositivity (i.e., either positive or negative for H. pylori) and serointensity (concentration of antibodies against H. pylori antigens) in adjusted models were associated with worse function on tasks of Numeric memory, Reasoning, and errors on the Pairs matching test but better function on the Tower rearrangement task. Together, these findings suggest that H. pylori seropositivity and serointensity might be associated with worse cognitive function in this age group.

In the increasingly challenging field of clinical microbiology, diagnosis is a cornerstone whose accuracy and timing are crucial for the successful management, therapy, and outcome of infectious diseases. Currently employed biomarkers of infectious diseases define the scope and limitations of diagnostic techniques. As such, expanding the biomarker catalog is crucial to address unmet needs and bring about novel diagnostic functionalities and applications.

This review describes the extracellular nucleases of 15 relevant bacterial pathogens and discusses the potential use of nuclease activity as a diagnostic biomarker. Articles were searched for in PubMed using terms: "nuclease", "bacteria", "nuclease activity" or "biomarker". For overview sections, original and review articles between 2000 and 2019 were searched for using terms: "infections", "diagnosis", "bacterial", "burden", "challenges". Informative articles were selected.

Using the catalytic activity of nucleases offers new possibilities compared to established biomarkers. Nucleic acid activatable reporters in combination with different transduction platforms and delivery methods can be used to detect disease-associated nuclease activity patterns in vitro and in vivo for prognostic and diagnostic applications. Even when these patterns are not obvious or of unknown etiology, screening platforms could be used to identify new disease reporters.

Co-infection between Helicobacter pylori (Hp) and groups of periodontal pathogens may alter the onset of Alzheimer's disease (AD) and all-cause dementia. We examined the interactive associations among Hp sero-positivity, periodontal disease (Pd), and infections with incident AD and all-cause dementia, among older adults (≥65 years at baseline). Up to 1431 participants from phase 1 of the National Health and Nutrition Survey III (1988-1991) had complete data till January 1st, 2014 on Hp sero-positivity with a mean follow-up of 10-11 years for AD and all-cause dementia incidence. Exposures consisted of 19 periodontal pathogens, constructed factors and clusters, and two Pd markers- probing depth and clinical attachment loss (CAL). Cox proportional hazards models were performed. Around 55% of the selected sample was Hp⁺. We found that Prevotella intermedia, Campylobacter Rectus, Factor 2 (Pi/Prevotella nigrescens/Prevotella melaninogenica), and the Orange-Red cluster interacted synergistically with Hp sero-positivity, particularly with respect to AD incidence. The presence of higher levels of Actinomyces Naeslundii (An) enhanced the effect of being Hp⁺ on both AD and all-cause dementia incidence. In contrast, Fusobacterim nucleatum (Fn), and Factor 1 (which included Fn), exhibited an antagonistic interaction with Hp in relation to all-cause dementia. Both probing depth and CAL had direct associations with all-cause dementia among Hp⁺ individuals, despite nonsignificant interaction. Selected periodontal pathogen titers, factors, and clusters interacted mostly synergistically, with Hp sero-positivity, to alter the risk of AD and all-cause dementia. Ultimately, a randomized controlled trial is needed, examining effects of co-eradication of Hp and select periodontal pathogens on neurodegenerative disease.

Bacterial extracellular vesicles (BEVs) have emerged as candidate signaling vectors for long-distance interkingdom communication within the gut-microbiota brain axis. Most bacteria release these nanosized vesicles, capable of signaling to the brain via their abundant protein and small RNA cargo, possibly directly via crossing the blood-brain barrier. BEVs have been shown to regulate brain gene expression and induce pathology at most stages of neuroinflammation and neurodegeneration, and thus they may play a causal role in diseases such as Alzheimer's, Parkinson's, and depression/anxiety. On the other hand, BEVs have intrinsic therapeutic properties that may be relevant to probiotic therapy and can also be engineered to function as drug delivery vehicles and vaccines. Thus, BEVs may be both a cause of and solution to neuropathological conditions. In this review, current knowledge of the physiological roles of BEVs as well as state of the art pertaining to the development of therapeutic BEVs in the context of the microbiome-gut-brain axis are summarized.

This review considers the data on Helicobacter pylori (H. pylori), which have been accumulated over 40 years since its description as an etiological factor in gastrointestinal diseases. The majority of modern publications are devoted to the study of the pathogenic properties of the microorganism in the development of chronic gastritis, peptic ulcer disease, and gastric cancer, as well as methods for its eradication. However, in recent years, there have been more and more studies which have suggested that H. pylori has a beneficial, or potentially positive, effect on the human body. The authors have attempted to objectively analyze the information accumulated in the literature on H. pylori. Some studies consider it as one of the recently identified human bacterial pathogens, and special attention is paid to the evidence suggesting that it is probably part of the composition of the human microbiome as a commensal (commensal from French to English is a table companion) or even a symbiont. The presented data discussing the presence or absence of the effect of H. pylori on human health suggest that there is an apparent ambiguity of the problem. The re-assessment of the data available on H. pylori infection is important in order to answer the question of whether it is necessary to create a program of mass H. pylori eradication or to apply a more personalized approach to treating patients with H. pylori-associated gastrointestinal diseases and to perform eradication therapy.

Parkinson's disease (PD) and Alzheimer's disease (AD) are the most common neurodegenerative disorders, with an overall global incidence of 40 million. Many studies have revealed the association of intestinal disorders and bacterial infections with PD, but few studies have found such a relationship with AD. In this meta-analysis, related articles published up to September 2018 were searched in PubMed. Of the 2121 related articles screened initially, 56 were found to be eligible. Data on the risks of PD and AD due to five intestinal disorders and infection with Helicobacter pylori, as a representative intestinal microbe, were obtained, and a fixed- or random-effects model was used to pool the odds ratios (ORs) with 95% confidence interval (CIs) from individual studies. The combined OR for all types of intestinal disorders with an increased risk of PD was 3.36 (95% CI: 2.70-4.17). The ORs for each category were as follows: constipation, 4.05 (95% CI, 3.24-5.06); inflammatory bowel disease (IBD), 1.16 (95% CI, 0.89-1.52); irritable bowel syndrome (IBS), 1.75 (95% CI, 0.55-5.56); small intestinal bacterial overgrowth, 5.15 (95% CI, 3.33-7.96); and diarrhea, 1.27 (95% CI, 0.28-5.75). The combined OR of all types of intestinal disorders with an increased risk of AD was 1.52 (95% CI, 1.09-2.13). The ORs for IBS and IBD were 1.42 (95% CI, 1.02-1.99) and 2.40 (95% CI, 1.00-5.76), respectively. The risk estimates of H. pylori infection in PD and AD patients were as follows: OR, 1.65 (95% CI, 1.43-1.91) and OR, 1.40 (95% CI, 1.12-1.76), respectively. These findings suggest that PD and AD are significantly associated with intestinal disorders. The negative roles of H. pylori in the development of PD or AD should be evaluated to shed new light on the diagnosis and treatment of PD and AD. National governments should periodically inspect the intestinal condition of residents and extend health plans to improve intestinal health to prevent potential neurological disorders.

Alzheimer's disease (AD) is an increasingly common neurodegenerative disease. Since the intestinal microbiome is closely related to nervous system diseases, alterations in the composition of intestinal microbiota could potentially contribute to the pathophysiology of AD. However, how the initial interactions with intestinal microbes alter events later in life, such as during neurodegenerative diseases, is still unclear. This review summarizes what is known about the relationship between the intestinal microbiome and AD.

Infectious agents were recently implicated in Alzheimer's disease (AD) and etiology of other dementias, notably Helicobacter pylori.

We tested associations of H. pylori seropositivity with incident all-cause and AD dementia and with AD-related mortality among US adults in a retrospective cohort study. Data from the National Health and Nutrition Surveys III, phase 1 (1988-1991) and 1999-2000 linked with Medicare and National Death Index registries, were used (baseline age ≥45 y, follow-up to 2013, N_pooled = 5927).

A positive association between H. pylori seropositivity and AD mortality was found in men (hazard ratio_{adj, pooled} = 4.33, 95% confidence interval: 1.51-12.41, P = .006), which was replicated for incident AD and all-cause dementia, with hazard ratio_{adj, pooled} = 1.45 (95% confidence interval: 1.03-2.04, P = .035) and hazard ratio_{adj, III} = 1.44 (95% confidence interval: 1.05-1.98, P = .022), respectively. These associations were also positive among higher socioeconomic status groups.

In sum, H. pylori seropositivity's direct association with AD mortality, all-cause dementia, and AD dementia was restricted to men and to higher socioeconomic status groups.

The gut microbiota comprises a complex community of microorganism species that resides in our gastrointestinal ecosystem and whose alterations influence not only various gut disorders but also central nervous system disorders such as Alzheimer's disease (AD). AD, the most common form of dementia, is a neurodegenerative disorder associated with impaired cognition and cerebral accumulation of amyloid-β peptides (Aβ). Most notably, the microbiota-gut-brain axis is a bidirectional communication system that is not fully understood, but includes neural, immune, endocrine, and metabolic pathways. Studies in germ-free animals and in animals exposed to pathogenic microbial infections, antibiotics, probiotics, or fecal microbiota transplantation suggest a role for the gut microbiota in host cognition or AD-related pathogenesis. The increased permeability of the gut and blood-brain barrier induced by microbiota dysbiosis may mediate or affect AD pathogenesis and other neurodegenerative disorders, especially those associated with aging. In addition, bacteria populating the gut microbiota can secrete large amounts of amyloids and lipopolysaccharides, which might contribute to the modulation of signaling pathways and the production of proinflammatory cytokines associated with the pathogenesis of AD. Moreover, imbalances in the gut microbiota can induce inflammation that is associated with the pathogenesis of obesity, type 2 diabetes mellitus, and AD. The purpose of this review is to summarize and discuss the current findings that may elucidate the role of the gut microbiota in the development of AD. Understanding the underlying mechanisms may provide new insights into novel therapeutic strategies for AD.

Helicobacter pylori has changed radically gastroenterologic world, offering a new concept in patients' management. Over time, more medical data gave rise to diverse distant, extragastric manifestations and interactions of the "new" discovered bacterium. Special interest appeared within the field of neurodegenerative diseases and particularly Alzheimer's disease, as the latter and Helicobacter pylori infection are associated with a large public health burden and Alzheimer's disease ranks as the leading cause of disability. However, the relationship between Helicobacter pylori infection and Alzheimer's disease remains uncertain.

We performed a narrative review regarding a possible connection between Helicobacter pylori and Alzheimer's disease. All accessible relevant (pre)clinical studies written in English were included. Both affected pathologies were briefly analyzed, and relevant studies are discussed, trying to focus on the possible pathogenetic role of this bacterium in Alzheimer's disease.

Data stemming from both epidemiologic studies and animal experiments seem to be rather encouraging, tending to confirm the hypothesis that Helicobacter pylori infection might influence the course of Alzheimer's disease pleiotropically. Possible main mechanisms may include the bacterium's access to the brain via the oral-nasal-olfactory pathway or by circulating monocytes (infected with Helicobacter pylori due to defective autophagy) through disrupted blood-brain barrier, thereby possibly triggering neurodegeneration.

Current data suggest that Helicobacter pylori infection might influence the pathophysiology of Alzheimer's disease. However, further large-scale randomized controlled trials are mandatory to clarify a possible favorable effect of Helicobacter pylori eradication on Alzheimer's disease pathophysiology, before the recommendation of short-term and cost-effective therapeutic regimens against Helicobacter pylori-related Alzheimer's disease.

The association of Helicobacter pylori (Hp) infection and Alzheimer's disease has widely been addressed, but no relative data exist regarding vascular dementia (VD). The purpose of this study was to evaluate the relationship between Hp infection and VD.

From January 2014 to March 2015, patients at Tai'an City Central Hospital who were diagnosed with VD were included. Patients were divided into Hp positive and Hp negative group using the (13)C-urea breath test ((13)C-UBT). Three inflammatory cytokines including interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were detected.

A total of 173 VD patients were included in the study. According to (13)C-UBT, 104 patients (60.1%) were Hp positive VD patients and 69 patients (39.9%) were Hp negative patients. No differences were found between Hp positive and Hp negative patients as regard to age, gender, body mass index, education level, hypertension, diabetes mellitus and hyperlipidemia (p > 0.05). Hp positive patients demonstrated significantly lower mean mini-mental state examination and Montreal cognitive assessment scores (p < 0.05) and higher plasma levels of IL-1β, IL-6 and TNF-α than Hp negative patients (p < 0.05).

Hp infection might contribute, at least in part, to the cognitive decline in patients with VD, and play a critical role possibly through increasing expression of IL-1β, IL-6 and TNF-α.

Despite recent research focus on the association between Helicobacter pylori (H. pylori) infection and multiple sclerosis (MS) there is no consensus about the findings. To obtain a more comprehensive estimate of the association we conducted a meta-analysis to determine the prevalence of H. pylori infection in MS patients and healthy controls. Pubmed and EMBASE were searched to identify eligible studies. Nine studies were selected for inclusion, involving 2806 cases (1553 patients with MS and 1253 controls). Overall, the prevalence of H. pylori infection in MS patients was lower than that in control groups (24.66% vs. 31.84%, OR=0.69, 95% CI: 0.57-0.83, P<0.0001). Subgroup analysis revealed that the levels of H.pylori infection among MS patients were lower than for control subjects in Western countries (11.90% vs. 16.08%, OR=0.63, 95% CI: 0.43-0.91, P=0.01), but were not statistically significant in Eastern countries (39.39% vs. 43.82%, OR=0.79, 95% CI: 0.55-1.14, P=0.20). Our data show that H. pylori infection and MS is negatively correlated, especially in Western countries. Whether H. pylori infection is a protective factor against MS risk should thus be addressed in large-scale and prospective studies.

At present, the clinical significance of Helicobacter pylori infection has been validly determined within the development of a diversity of gastroduodenal diseases, including chronic gastritis, gastroduodenal ulcer, MALT lymphoma, and gastric adenocarcinoma. The Expert Council's Maastricht IV consensus (2010) determining international standards for the diagnosis and treatment of H. pylori infection is that there is evidence that the latter may be associated with the development of a number of extragastroduodenal diseases (EGDDs) presented by iron-deficiency anemia of unspecified etiology, idiopathic thrombocytopenic purpura, and vitamin B12 deficiency. In these diseases, it is recommended that infection with H. pylori be diagnosed and, if the test is positive, this microorganism be eradicated. A large number of investigations have been recently conducted to examine the association of H. pylori infection with other EGDDs. This paper reviews theoretical and epidemiological data on the association of H. pylori with diseases of the cardiovascular (atherosclerosis, myocardial infarction) and central nervous (Alzheimer's disease, Parkinson's disease) systems, pancreas (autoimmune pancreatitis, pancreatic cancer), oncological (colonic adenomas, colorectal cancer, hepatocellular carcinoma), dermatological (chronic spontaneous urticaria), and other EGDDs. The review highlights the potential protective role of H. pylori in diseases with the atopic element of genesis and a complicated course of gastroesophageal reflux disease (Barrett's esophagus, esophageal adenocarcinoma).

The isolation of Helicobacter pylori from the human stomach produced significant changes in how gastroenterologists, immunologists, epidemiologists, pathologists and microbiologists have approached gastro-duodenal diseases in the last half of the XX century. However, research of this organism has progressed greatly in the first decade of this century, evidence suggest that H. pylori is associated with disease only in humans older than 40 years, while, the lack of H. pylori colonization is associated with the emergence of new diseases, particularly in younger individuals. These differing effects of H. pylori colonization have created two contrasting concepts: the 'bad' and the 'good' Helicobacter. Following from renewed interest in the normal human microbiome, we need to reconsider our definitions and perhaps recognize that H. pylori might be a normal member of the human gastric microbiome in ancient humans that gradually, as results of the improvement in our environment, is disappearing.

Alzheimer's disease (AD) is a neurodegenerative condition that occurs in two forms, an early-onset form that is genetically determined and a far more common late-onset form that is not. In both cases, the disease results in severe cognitive dysfunction, among other problems, and the late-onset form of the disease is now considered to be the most common cause of dementia among the elderly. While a good deal of research has been focused on elucidating the etiology of the late-onset form for more than two decades, results to date have been modest and have not yet engendered useful therapeutic strategies for cure of the disease. In this review, we discuss the prevalent ideas that have governed this research for several years, and we challenge these ideas with alternative findings suggesting a multifactorial etiology. We review promising newer ideas that may prove effective as therapeutic interventions for late-onset AD, as well as providing reliable means of earlier and more specific diagnosis of the disease process. In the discussions included here, we reference relevant clinical and basic science literature underlying research into disease etiology and pathogenesis, and we highlight current reviews on the various topics addressed.

The discovery of the C9ORF72 hexanucleotide repeat expansion in 2011 and the immediate realisation of a remarkably high prevalence in both familial and sporadic frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) triggered an explosion of interest in studies aiming to define the associated clinical and investigation phenotypes and attempts to develop technologies to measure more accurately the size of the repeat region. This article reviews progress in these areas over the subsequent 2 years, focussing on issues directly relevant to the practising physician. First, we summarise findings from studies regarding the global prevalence of the expansion, not only in FTLD and ALS cases, but also in other neurological diseases and its concurrence with other genetic mutations associated with FTLD and ALS. Second, we discuss the variability in normal repeat number in cases and controls and the theories regarding the relevance of intermediate and pathological repeat number for disease risk and clinical phenotype. Third, we discuss the usefulness of various features within the FTLD and ALS clinical phenotype in aiding differentiation between cases with and without the C9ORF72 expansion. Fourth, we review clinical investigations used to identify cases with the expansion, including neuroimaging and cerebrospinal fluid markers, and describe the mechanisms and limitations of the various diagnostic laboratory techniques used to quantify repeat number in cases and controls. Finally, we discuss the issues surrounding accurate clinical and technological diagnosis of patients with FTLD and/or ALS associated with the C9ORF72 expansion, and outline areas for future research that might aid better diagnosis and genetic counselling of patients with seemingly sporadic or familial FTLD or ALS and their relatives.

In the last year, several diseases from outside of the gastrointestinal tract have been associated with Helicobacter pylori infection. Indeed, this bacterium produces a low-grade inflammatory state, induces molecular mimicry mechanisms, and interferes with the absorbance of nutrients and drugs possibly influencing the occurrence or the evolution of many diseases. In addition to its role in some hematologic conditions, such as immune thrombocytopenic purpura, idiopathic sideropenic anemia, and vitamin B12 deficiency, which were included in the current guidelines, several other conditions such as cardiovascular diseases, diabetes mellitus, hepatobiliary diseases, and neurologic disorders have also shown promising results.

Helicobacter pylori seropositivity is a potential risk for poor cognition among US adults.

Cross-sectional data from the National Health and Nutrition Examination Survey III, Phase 1 (1988-1991), were used. Measures included age group-specific neuropsychological test batteries and two measures of H. pylori seropositivity (immunoglobulin G [IgG] and IgG CagA) (20-59 years old: n = 2090-2,248; 60-90 years old: n = 2123-2388). We explored sex- and race-specific associations.

Using multiple ordinary least square and zero-inflated Poisson regression models, we detected a poorer performance among those 60-90 years old with H. pylori IgG+ versus IgG- on a verbal memory test (story recall, correct items), overall (β = -0.04 [0.01], p = .010). Non-Hispanic (NH) blacks and women (20-59 years old) performed worse on the serial digits learning total errors (SDL-TE) when H. pylori IgG+ (versus IgG-), another verbal memory test (β = +0.94 [0.40; p = .029] and β = +1.19 [0.44; p = .012], respectively; p<.10 for interaction by sex and race). More trials to completion on this test (SDL-TTC) were also required among H. pylori IgG+ overall (20-59 years old; β = +0.30 [0.13], p = .033). Other race-specific associations without significant interaction by race were detected in the same direction of worse performance with seropositivity in all three major race groups and for both age categories, covering several domains of cognition.

H. pylori seropositivity markers were associated with poor cognition among US adults. Longitudinal research is needed to extrapolote those findings to cognitive decline, incident dementia, and Alzheimer's disease.