BACKGROUND: Toxoplasma gondii infection of Alzheimer\'s disease model mice decreases amyloid β plaques. We aimed to determine if there is a brain regional difference in amyloid β reduction in the brains of T. gondii-infected compared to control mice.
METHODS: Three-month-old 5xFAD (AD model) mice were injected with T. gondii or with phosphate-buffered saline as a control. Intact brains were harvested at 6 weeks postinfection, optically cleared using iDISCO+, and brain-wide amyloid burden was visualized using volumetric light-sheet imaging. Amyloid signal was quantified across each brain and computationally mapped to the Allen Institute Brain Reference Atlas to determine amyloid density in each region.
RESULTS: A brain-wide analysis of amyloid in control and T. gondii-infected 5xFAD mice revealed that T. gondii infection decreased amyloid burden in the brain globally as well as in the cortex and hippocampus, and many daughter regions. Daughter regions that showed reduced amyloid burden included the prelimbic cortex, visual cortex, and retrosplenial cortex. The olfactory tubercle, a region known to have increased monocytes following T. gondii infection, also showed reduced amyloid after infection.
CONCLUSIONS: T. gondii infection of AD mice reduces amyloid burden in a brain region-specific manner that overlaps with known regions of T. gondii infection and peripheral immune cell infiltration.

BACKGROUND: Children diagnosed with subacute sclerosing panencephalitis (SSPE) display a range of neuroimaging abnormalities during different stages of the disease, but their exact clinical significance remains unclear.
METHODS: In this retrospective cohort study, our objective was to examine magnetic resonance imaging (MRI) abnormalities in the brains of patients aged 18 years or younger with subacute sclerosing panencephalitis. We aimed to correlate these MRI abnormalities with clinical severity, sociodemographic variables, electroencephalographic (EEG) abnormalities, and cerebrospinal anti-measles antibody titers.
RESULTS: The study included 112 cases of subacute sclerosing panencephalitis (mean age at onset: 8.9 ± 2.6 years). MRI analysis at the time of presentation revealed the following abnormalities: subcortical white matter signal changes (n = 95), periventricular white matter signal changes (n = 76), splenium of corpus callosum involvement (n = 39), diffuse corpus callosum involvement (n = 27), cerebral atrophy (n = 35), basal ganglia involvement (n = 10), and brain stem involvement (n = 2). Notably, subcortical white matter involvement, periventricular white matter involvement, diffuse corpus callosum involvement, and basal ganglia involvement were more prevalent in patients with stage III and IV subacute sclerosing panencephalitis (P < .05 for all). Cerebral atrophy was also significantly more common in patients with stage III compared to those with stage IV subacute sclerosing panencephalitis (P < .0001). However, no substantial positive or negative associations were found between MRI findings and EEG abnormalities, other sociodemographic/clinical variables, and cerebrospinal fluid measles-specific antibody titers (P > .05).
CONCLUSIONS: Early in the disease progression of subacute sclerosing panencephalitis, the temporoparietal and parietooccipital regions of the subcortical white matter are affected. Neuroimaging abnormalities exhibit a stronger association with Jabbour\'s clinical staging, but do not show significant associations with other clinical, sociodemographic, and EEG features.

Three-dimensional culture models of the brain enable the study of neuroinfection in the context of a complex interconnected cell matrix. Depending on the differentiation status of the neural cells, two models exist: 3D spheroids also called neurospheres and cerebral organoids. Here, we describe the preparation of 3D spheroids and cerebral organoids and give an outlook on their usage to study Rift Valley fever virus and other neurotropic viruses.

Pott\'s puffy tumors are assumed to be infrequent concomitant intra- and extracranial abscesses, mainly secondary to complicated frontal sinusitis during infancy. Due to the close proximity to the superior sagittal sinus, there is a risk of developing venous infections, thrombosis, and morbidity. In this case report, we present a case of an 11-year-old girl who presented with headache and face edema. After recognizing the Pott\'s puffy tumor pattern on the CT scan and brain MRI, the neurosurgical approach involved pus evacuation and frontal sinus blockage, and the patient received antibiotic therapy and was evaluated for total recovery. To our knowledge, the prompt diagnosis and treatment of such conditions are paramount to avoid complications, and differential diagnosis should be encouraged in medical practice.

Listeria monocytogenes is a Gram-positive facultative anaerobic bacterium that is ubiquitous in the environment and can cause severe infections in immunocompromised individuals, pregnant women, and newborns. Listeriosis can manifest as meningitis, encephalitis, or sepsis, and its diagnosis requires a high index of suspicion. The case is reported of a rare presentation of rhombencephalitis by listeriosis in a 61-year-old male who initially suffered from subacute gastric disturbances and fever. Neurological consultation showed abnormal functions of cranial nerves and meningeal signs were observed. MRI revealed a poorly demarcated focus of approximately 45 × 16 × 15mm, indicating possible inflammatory processes, necessitating a lumbar puncture. Assessment of the CSF indicated infection with the bacterium- Listeria Monocytogenes, with the final diagnosis of Listeriosis encephalitis. Despite antibiotic therapy of Ceftazidine and Ampicillin, the patient\'s condition deteriorated, followed by death.

UNASSIGNED: The aim of this study was to characterise long-term neurological and neurocognitive sequelae after tick-borne encephalitis (TBE) in adults.
UNASSIGNED: 98 prospective consecutive TBE patients, classified by disease severity, were included. Immediate outcomes were evaluated with Glasgow Outcome Scale (GOS) and Rankin Scale (RS). After 6 and 18 months, long-term disability was evaluated using Modified Rankin Scale (MRS) and neurocognitive assessment was performed with Matrics Consensus Cognitive Battery (MCCB), measuring processing speed, attention/vigilance, working memory, verbal learning, visual learning, reasoning/problem solving and social cognition. The MCCB results were compared to healthy age, gender and education-matched controls.
UNASSIGNED: Mild, moderate, and severe TBE was diagnosed in 53.1%, 38.8%, and 8.2% of cases, respectively. At discharge, 25.5% of the patients had major or moderate impairments (GOS) and various levels of disability in 34.7% (RS). Up to 18 months from the onset of TBE, over 20% remained with slight to moderate disability (MRS). GOS, RS and MRS scores correlated with disease severity. At 6 months after the onset, TBE patients scored significantly lower than controls in processing speed, verbal, and visual learning. Two latter domains were significantly more impaired in patients with mild TBE. Patients aged 18-39 performed significantly worse in attention/vigilance and working memory, whereas aged 60+ in verbal learning. A year later, significant improvement was observed in six of seven cognitive domains.
UNASSIGNED: Long-term neurological sequelae persist in a substantial proportion of TBE patients with significant impairment in several cognitive domains, especially in younger patients and even after mild TBE.

The highly prevalent herpes simplex virus type 1 (HSV-1) causes a range of diseases, including cold sores, blinding keratitis, and life-threatening encephalitis. HSV-1 initially replicates in epithelial cells, enters the peripheral nervous system via neurites, and establishes lifelong infection in the neuronal cell bodies. Neurites are highly dynamic structures that grow or retract in response to attractive or repulsive cues, respectively. Here, we show that infection with HSV-1, but not with a mutant virus lacking glycoprotein G (gG), reduced the repulsive effect of epithelial cells on neurite outgrowth and facilitated HSV-1 invasion of neurons. HSV-1 gG was required and sufficient to induce neurite outgrowth by modifying the protein composition of extracellular vesicles, increasing the amount of neurotrophic and neuroprotective proteins, including galectin-1. Antibodies directed against galectin-1 neutralized the capacity of extracellular vesicles released from HSV-1-infected cells to promote neurite outgrowth. Our study provides new insights into the neurotropism of HSV-1 and identifies a viral protein that modifies the protein composition of extracellular vesicles to stimulate neurite outgrowth and invasion of the nervous system.IMPORTANCEHerpes simplex virus type 1 (HSV-1) must infect neurites (or nerve endings) to establish a chronic infection in neurons. Neurites are highly dynamic structures that retract or grow in the presence of repulsive or attractive proteins. Some of these proteins are released by epithelial cells in extracellular vesicles and act upon interaction with their receptor present on neurites. We show here that HSV-1 infection of epithelial cells modulated their effect on neurites, increasing neurite growth. Mechanistically, HSV-1 glycoprotein G (gG) modifies the protein composition of extracellular vesicles released by epithelial cells, increasing the amount of attractive proteins that enhance neurite outgrowth and facilitate neuronal infection. These results could inform of therapeutic strategies to block HSV-1 induction of neurite outgrowth and, thereby, neuronal infection.

Cerebral abscess is an uncommon complication of cyanotic heart disease. However, it has a high case fatality rate, and its management requires a multidisciplinary approach. Earlier diagnosis would result in a better outcome. In this report, we presented a case of a 6-year-old boy with a cerebral abscess and a large ventricular septal defect, which was treated surgically in a rural area with a limited resources facility.

Brain abscesses are localized infections in the brain\'s parenchyma, characterized by inflammation, pus formation, and the development of a surrounding capsule. These lesions typically occur due to underlying factors such as immunosuppression, ear and sinus infections, and contamination during neurosurgery. While brain abscesses are a life-threatening complication of cyanotic heart defects, they are rarely reported, with only sporadic cases previously documented. This article presents the case of an eight-year-old male patient with an uncorrected transposition of the great arteries, who was evaluated for symptoms including headache, fever, and neurological focalization. Diagnostic imaging revealed three lesions consistent with brain abscesses. Furthermore, the causal agents were identified as Streptococcus intermedius and Fusobacterium spp., representing oral microorganisms. Additionally, the patient exhibited poor oral hygiene and dental caries in multiple teeth. This article discusses and integrates the possible pathophysiological mechanisms that allowed a localized dental infection to spread hematogenously and cause brain abscesses in this patient. Prompt management of the infectious source is crucial to prevent a poor prognosis associated with brain abscesses. Therefore, this case emphasizes the importance of regular dental assessments and thromboprophylaxis for patients with underlying cardiomyopathies that cause right-to-left shunting to prevent potential complications.

Few cases of disease by Kocuria kristinae have been reported, some in immunocompetent patients but mainly in immunocompromised. The current case report describes a 28-year-old female with an initial diagnosis of pituitary macroadenoma. After the initial surgery, the patient was readmitted due to tension pneumocephalus and cerebrospinal fluid (CSF) fistula. Cultures showed K. kristinae in the CSF and Candida albicans in the urine. The patient died after multiple complications. This is the first case of neuroinfection by K. kristinae in the American continent as reviewed. It was not determined as the main cause of death due to the sudden herniation, however, with active infection derived from the identification in two different samples, for this reason, we consider that it could be useful to take it as a cause of disease and a probable cause when the studies for detection of the most common pathogens have been negative.