Lyme disease (LD) spirochetes are well known to be able to disseminate into the tissues of infected hosts, including humans. The diverse strategies used by spirochetes to avoid the host immune system and persist in the host include active immune suppression, induction of immune tolerance, phase and antigenic variation, intracellular seclusion, changing of morphological and physiological state in varying environments, formation of biofilms and persistent forms, and, importantly, incursion into immune-privileged sites such as the brain. Invasion of immune-privileged sites allows the spirochetes to not only escape from the host immune system but can also reduce the efficacy of antibiotic therapy. Here we present a case of the detection of spirochetal DNA in multiple loci in a LD patient's post-mortem brain. The presence of co-infection with sensu stricto and in this LD patient's brain was confirmed by PCR. Even though both spirochete species were simultaneously present in human brain tissue, the brain regions where the two species were detected were different and non-overlapping. The presence of atypical spirochete morphology was noted by immunohistochemistry of the brain samples. Atypical morphology was also found in the tissues of experimentally infected mice, which were used as a control.
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http://dx.doi.org/10.3390/ijms242316906 | DOI Listing |
Trends Immunol
December 2024
Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland. Electronic address:
Diverse macrophage populations inhabit the rodent and human central nervous system (CNS), including microglia in the parenchyma and border-associated macrophages (BAMs) in the meninges, choroid plexus, and perivascular spaces. These innate immune phagocytes are essential in brain development and maintaining homeostasis, but they also play diverse roles in neurological diseases. In this review, we highlight the emerging roles of CNS macrophages in regulating vascular function in health and disease.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois, USA.
Introduction: Type 2 diabetes increases the risk of Alzheimer's disease (AD) dementia. Insulin signaling dysfunction exacerbates tau protein phosphorylation, a hallmark of AD pathology. However, the comprehensive impact of diabetes on patterns of AD-related phosphoprotein in the human brain remains underexplored.
View Article and Find Full Text PDFBMJ Ment Health
December 2024
Research Center for Child Mental Development, University of Fukui, Fukui, Japan.
Question: Cognitive-behavioural therapy (CBT) is frequently implemented for individuals with attention-deficit hyperactivity disorder (ADHD). It is still unknown which specific components are effective, because CBT is a complex intervention with several components. The objective of this review was to assess the efficacy of CBT components for ADHD.
View Article and Find Full Text PDFMol Cell Neurosci
December 2024
Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Türkiye; Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir, Türkiye; Department of Neuroscience, Institute of Health Sciences, Dokuz Eylul University, Izmir, Türkiye. Electronic address:
Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the accumulation of amyloid plaques, phosphorylated tau tangles and microglia toxicity, resulting in neuronal death and cognitive decline. Since microglia are recognized as one of the key players in the disease, it is crucial to understand how microglia operate in disease conditions and incorporate them into models. The studies on human microglia functions are thought to reflect the post-symptomatic stage of the disease.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
December 2024
Department of Psychiatry, University of Cambridge, Cambridge, UK; Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany. Electronic address:
Background: A preference for sooner-smaller over later-larger rewards, known as delay discounting, is a candidate transdiagnostic marker of waiting impulsivity and a research domain criterion. While abnormal discounting rates have been associated with many psychiatric diagnoses and abnormal brain structure, the underlying neuropsychological processes remain largely unknown. Here, we deconstruct delay discounting into choice and rate processes by testing different computational models and investigate their associations with white matter tracts.
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