Teresa Wierzba-Bobrowicz

Not available Keywords: JCV PML neuropathology ultrastructure

Alzheimer's disease is a progressive neurodegenerative disorder that disrupts the brain regions involved in memory and cognitive functions. This impairment ultimately results in severe deficits in memory, learning, reasoning, communication, and the ability to perform daily activities. Our research reveals a statistically significant decrease in the density of neural progenitor cells within the dentate gyrus of the hippocampus and the subventricular zone of the lateral ventricles in patients diagnosed with Alzheimer's disease. This reduction correlates with the disease's progression. As Alzheimer’s disease advances, cognitive functions decline progressively, leading to the identification of five distinct stages of β-amyloid distribution across various brain structures. Early symptoms include short-term memory deficits and learning difficulties, along with cognitive, psychiatric, and neurological disturbances. Given the hippocampus's essential role in these functions, one would expect to see substantial changes in this brain region. Thus, understanding adult neurogenesis is vital in Alzheimer’s disease, particularly since the hippocampus, a primary neurogenic area, is notably impacted in affected individuals.

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with the onset of neurological and psychiatric symptoms during and after the acute phase of illness. Inflammation and hypoxia induced by SARS-CoV-2 affect brain regions essential for fine motor function, learning, memory, and emotional responses. The mechanisms of these central nervous system symptoms remain largely unknown. While looking for the causes of neurological deficits, we conducted a study on how SARS-CoV-2 affects neurogenesis. In this study, we compared a control group with a group of patients diagnosed with COVID-19. Analysis of the expression of neurogenesis markers showed a decrease in the density of neuronal progenitor cells and newborn neurons in the SARS-CoV-2 group. Analysis of COVID-19 patients revealed increased microglial activation compared with the control group. The unfavorable effect of the inflammatory process in the brain associated with COVID-19 disease increases the concentration of cytokines that negatively affect adult human neurogenesis.

The increased life expectancy of individuals with Down syndrome (DS) is associated with increased prevalence of trisomy 21–linked early-onset Alzheimer’s disease (EOAD) and dementia. The aims of this study of 14 brain regions including the entorhinal cortex, hippocampus, basal ganglia, and cerebellum in 33 adults with DS 26–72 years of age were to identify the magnitude of brain region–specific developmental neuronal deficits contributing to intellectual deficits, to apply this baseline to identification of the topography and magnitude of neurodegeneration and neuronal and volume losses caused by EOAD, and to establish age-based staging of the pattern of genetically driven neuropathology in DS. Both DS subject age and stage of dementia, themselves very strongly correlated, were strong predictors of an AD-associated decrease of the number of neurons, considered a major contributor to dementia. The DS cohort was subclassified by age as pre-AD stage, with 26–41-year-old subjects with a full spectrum of developmental deficit but with very limited incipient AD pathology, and 43–49, 51–59, and 61–72-year-old groups with predominant prevalence of mild, moderately severe, and severe dementia respectively. This multiregional study revealed a 28.1% developmental neuronal deficit in DS subjects 26–41 years of age and 11.9% AD-associated neuronal loss in DS subjects 43–49 years of age; a 28.0% maximum neuronal loss at 51–59 years of age; and a 11.0% minimum neuronal loss at 61–72 years of age. A total developmental neuronal deficit of 40.8 million neurons and AD-associated neuronal loss of 41.6 million neurons reflect a comparable magnitude of developmental neuronal deficit contributing to intellectual deficits, and AD-associated neuronal loss contributing to dementia. This highly predictable pattern of pathology indicates that successful treatment of DS subjects in the fourth decade of life may prevent AD pathology and functional decline.

Background: Homicide combined with subsequent suicide of the perpetrator is a particular form of interpersonal violence and, at the same time, a manifestation of extreme aggression directed against oneself. Despite the relatively well-described individual acts of homicide and suicide, both in terms of psychopathology and law, acts of homicide and subsequent suicide committed by the same person are not well-studied phenomena. The importance of emotional factors, including the influence of mental state deviations (psychopathology), on this phenomenon, is discussed in the literature, but still there is relatively little data with which to attempt neuropathological assessments of the brains of suicide killers. This paper is dedicated to the issue based on the neuropathological studies performed. Methods: We analyzed a group of murder–suicides using histochemical and immunohistochemical methods. Results: The results of our research indicate the presence of neurodegenerative changes including multiple deposits of ß-amyloid in the form of senile/amyloid plaques and perivascular diffuse plaques. Conclusions: Neurodegenerative changes found in the analyzed brains of suicide killers may provide an interesting starting point for a number of analyses. The presence of neurodegenerative changes at such a young age in some murderers may suggest preclinical lesions that affect cognitive functions and are associated with depressed moods.

Chordoid meningioma is an uncommon histopathological type of meningioma, frequently associated with Castleman's syndrome. Histologically, chordoid meningiomas are similar to chordomas. Because of their high proliferative index, they present aggressive biological behavior and high risk of postoperative recurrence. We report a case of choroid meningioma in adult patient without Castleman's syndrome manifestation. As its chordoid features is related with a rapid recurrence after incomplete removal, meticulous histopathological examination is crucial for the adequate postoperative treatment plan.

Herpes simplex encephalomyelitis (HSE) is a rare disease with a high mortality rate. Correct diagnosis is established on the basis of the combination of the clinical and investigative features. Unfortunately, precise diagnosis remains difficult due to several clinical similarities and false...