Abstract Quantitative analysis of positron emission tomography (PET) neuroimaging data is essential for studying neurodegenerative diseases, yet existing processing pipelines often rely on computationally intensive software packages such as FreeSurfer, limiting accessibility for many research groups. Here I introduce BrainPET Studio, an open-source desktop application for atlas-based regional PET quantification that operates entirely in Montreal Neurological Institute (MNI) standard space. BrainPET Studio integrates affine registration, optional Müller-Gartner (MG) partial volume correction (PVC), interactive quality control (QC), and standardized uptake value ratio (SUVR) calculation into a single graphical user interface (GUI), eliminating the requirement for FreeSurfer-based cortical reconstruction. I validated BrainPET Studio against two established pipelines: (1) the UC Berkeley Alzheimer’s Disease Neuroimaging Initiative (ADNI) AV1451 (flortaucipir) pipeline, which employs FreeSurfer v7.1.1 parcellation, SPM-based coregistration, and Geometric Transfer Matrix (GTM) PVC in native subject space; and (2) the volBrain/petBrain online platform. Region-of-interest (ROI) SUVR values were compared across 322 subjects. Overall Pearson correlation coefficients for meta-ROI composites ranged from r = 0.83–0.96 versus ADNI and r = 0.86–0.94 versus volBrain/petBrain. Detailed per-subject validation on four representative cases across 112 FreeSurfer-defined regions demonstrated strong agreement for large cortical composites and acceptable variability for smaller medial temporal structures. These results establish BrainPET Studio as a reliable, accessible, and extensible tool for multi-site PET research, educational applications, and studies where FreeSurfer-based processing is impractical.
Introduction: Listeria monocytogenes is a rare cause of neurological complications and is not known to affect the peripheral nervous system (PNS). We present a case of acute motor axonal neuropathy (AMAN) associated with Listeria monocytogenes infection.Case Presentation: A 60-year-old man developed progressive, symmetric, ascending weakness over one week, along with severe constipation. He had no history of trauma, infection, or vaccination but lived in precarious conditions. Neurological examination revealed multiple cranial nerve palsies, flaccid tetraparesis, absent reflexes, and albumin-cytologic dissociation in cerebrospinal fluid (CSF). Initial diagnosis was Guillain-Barré syndrome (GBS), and intravenous immunoglobulin (IVIg) was initiated. However, the patient showed no improvement and developed respiratory failure, requiring mechanical ventilation. Extensive workup, including PCR analysis of CSF, identified Listeria monocytogenes. Nerve conduction studies confirmed AMAN. The patient was treated with a 21-day course of intravenous ampicillin, leading to neurological stabilization and eventual full recovery after six months.Conclusion: This case highlights Listeria monocytogenes as a potential infectious cause of acute polyneuropathy, particularly in individuals with poor living conditions. It also raises the possibility of direct axonal damage by the bacterium. Early recognition and targeted antibiotic therapy may improve outcomes in similar cases.
This case report describes the clinical profile of a four-year-old male presenting with multiple developmental delays, including cognitive impairment, speech delay, and hyperactivity, following an episode of neonatal hypocalcemia. Born full-term via cesarean section after an uneventful pregnancy, the child exhibited delayed initiation of crying, requiring NICU observation. Early feeding difficulties and a diagnosis of hypocalcemia were noted. By the age of two and a half, parental concerns escalated regarding poor attention span, speech unintelligibility, and delayed social communication. Although gross motor milestones were achieved on time, the child showed significant deficits in language processing, attention regulation, and adaptive skills, including feeding and toilet training. Symptoms aligned with Attention-Deficit/Hyperactivity Disorder (ADHD) were evident, and minimal progress was seen despite therapeutic intervention. The clinical presentation suggests the possibility of an underlying neurogenetic syndrome, such as 22q11.2 deletion syndrome. This case emphasizes the importance of considering metabolic and genetic etiologies in the differential diagnosis of developmental delay. Early identification and multidisciplinary management are critical for improving long-term functional outcomes in children with complex neurodevelopmental disorders.
Cerebral small vessel disease (CSVD) comprises a spectrum of pathological processes that injure arterioles, capillaries and venules within the brain. Traditionally recognised as a vascular cause of lacunar stroke and vascular cognitive impairment, CSVD is now appreciated as a pervasive, age‑related substrate that converges with canonical proteinopathies to shape the clinical course of many neurodegenerative disorders. Emerging imaging, fluid biomarker and neuropathological data demonstrate that white‑matter hyperintensities, microinfarcts, microbleeds, enlarged perivascular spaces and microvascular blood‑brain‑barrier (BBB) failure accelerate amyloid‑β deposition, tau propagation, α‑synuclein aggregation and neuroinflammation. CSVD thereby lowers brain resilience, hastens cognitive and motor decline, and complicates therapeutic response in Alzheimer’s disease (AD), Parkinson’s disease (PD), dementia with Lewy bodies (DLB), frontotemporal degeneration (FTD) and mixed dementias. This narrative review (≈3000 words) summarises epidemiology, mechanistic links, imaging and fluid correlates, disease‑specific evidence, and therapeutic prospects, contending that CSVD represents a tractable target for delaying or preventing neurodegeneration.
Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by impairments in communication, social interaction, and repetitive behaviors. While its precise etiology remains elusive, emerging evidence highlights the pivotal role of oxidative stress and mitochondrial dysfunction in ASD pathophysiology. Oxidative stress refers to the imbalance between reactive oxygen species (ROS) production and the body’s antioxidant defenses, leading to cellular and molecular damage. This imbalance has been implicated in neural inflammation, neurotransmitter dysregulation, and impaired neuronal connectivity observed in ASD. Antioxidants, both endogenous and exogenous, play a critical role in neutralizing ROS and mitigating oxidative stress. Various studies suggest that antioxidant therapies, such as supplementation with glutathione, N-acetylcysteine (NAC), and vitamins C and E, may have therapeutic potential in reducing ASD-associated symptoms by targeting oxidative stress pathways. Preclinical and clinical evidence also underscores their potential to modulate mitochondrial function, reduce neuroinflammation, and regulate the gut-brain axis, which is often altered in ASD. This review aims to critically evaluate the role of oxidative stress in ASD, the biological mechanisms by which antioxidants act, and the current clinical evidence supporting their use in ASD management. It will further explore specific pathways targeted by antioxidants and discuss limitations and future research directions in this emerging field. By synthesizing existing evidence, this review seeks to provide a comprehensive understanding of how antioxidants could complement existing ASD treatments.
