Background/objective: Studies suggest that the neutrophil/lymphocyte ratio (NLR) may be a prognostic marker for different diseases with inflammatory components. This study aimed to quantify the NLR in individuals affected by different subtypes and severities of ischemic stroke and associated it with risk factors and treatment, and compared the results with data from healthy individuals. Methods: Clinical and laboratory data from medical records of patients over 18 years of age, victims of ischemic stroke, were collected. Data included leukocyte count and subtype, topography, risk factors, treatment and severity of stroke. For comparison, the number of leukocytes in healthy individuals was also quantified. NLR was determined by dividing the number of neutrophils by the number of lymphocytes. Results: A total of 218 patients were included, 194 stroke patients and 24 healthy individuals. Among all stroke patients, 45% had NLR values > 4 and 35% had values between 2 and 4; otherwise, 71% of healthy individuals had NRL < 2. The data also showed that the greater the severity of the stroke, measured by the NIHSS scale, the higher the NLR, at 24 and 72 h after the stroke. Among the stroke subtypes evaluated, the one with the lowest NLR values was small vessel stroke. Finally, the risk factors for stroke, its topography and treatment were not associated with NLR values. Conclusions: NLR is associated with stroke severity but does not correlate with stroke risk factors, topography, and treatment. The NLR may serve as a marker of stroke severity.

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are progressive neurodegenerative diseases with unclear etiology. Mutations in the TBK1 gene are associated with an increased risk of both FTD and ALS, presenting a diverse phenotype that includes the behavioral variant of FTD, primary progressive aphasia, and pure ALS. This mutation is rare, and to date, only one case report on TBK1-related clinical manifestations has been published in Brazil. Objective: To investigate the association between TBK1 gene mutations and the clinical manifestations of FTD and ALS in a Brazilian family, documenting the clinical history and disease progression of three first-degree relatives. Additionally, to conduct a literature review to better understand the impact of this mutation and its implications for neurological practice. Methods: Clinical data were collected from three patients in the same family who were receiving care at Dom Pedro II Geriatric Hospital and Central Hospital of the Irmandade da Santa Casa de Misericordia de São Paulo, including information on clinical symptoms, disease progression, and complementary exams — particularly genetic testing to detect and confirm the diagnosis. A detailed analysis of the existing literature on the disease was also conducted to better understand the implications of this mutation. Results: Three siblings affected by the TBK1 gene mutation were documented, with a unique family history suggesting that this genetic alteration has affected the lineage for several generations. Conclusion: Although rare, frontotemporal dementia with accompanying motor deficits is of significant relevance to neurologists due to its poor prognosis and the potential familial impact on descendants.

Background/Objectives: Banisteriopsis caapi contains β-carboline alkaloids with neuropharmacological and immunomodulatory properties, but their effects during prolonged exposure in established amyloid pathology remain poorly characterized. This study investigated whether chronic intermittent B. caapi administration modifies behavioral performance, fibrillar amyloid pathology, and hippocampal microglial alterations in aged PDGFB-APPSwInd mice. Methods: Male wild-type (WT) and PDGFB-APPSwInd transgenic (TG) mice aged 15–18 months received B. caapi extract (1.5 mL/kg, oral gavage) or vehicle twice weekly for four weeks. Locomotor activity, anxiety-like behavior, and spatial recognition memory were assessed using the open-field, elevated-plus-maze, and object-location tests, respectively. Hippocampal fibrillar amyloid plaques were evaluated by Thioflavin-S staining, and microglial immunoreactivity and morphology were assessed using Iba1 immunofluorescence and morphometric analysis. Results: Chronic B. caapi administration did not consistently modify locomotor activity, anxiety-like behavior, or spatial recognition memory. In TG mice, treatment increased the number of hippocampal Thioflavin-S-positive fibrillar amyloid plaques, without corresponding changes in total Thioflavin-S-positive area or median plaque size. Microglial alterations were predominantly genotype-associated, with TG mice exhibiting changes in Iba1-labeled cell quantification and morphology, particularly in the CA1 region. B. caapi treatment did not significantly modify these genotype-associated morphological alterations. Conclusions: Chronic intermittent B. caapi exposure was associated with a selective change in fibrillar amyloid plaque number without parallel changes in plaque area, plaque size, behavioral performance, or microglial morphology. These findings expand current evidence regarding the biological effects of repeated B. caapi exposure in the context of established amyloid pathology.