A Quantitative Comparison Between Human and Artificial Intelligence in the Detection of Focal Cortical Dysplasia.

Objectives: Artificial intelligence (AI) is thought to improve lesion detection. However, a lack of knowledge about human performance prevents a comparative evaluation of AI and an accurate assessment of its impact on clinical decision-making. The objective of this work is to quantitatively evaluate the ability of humans to detect focal cortical dysplasia (FCD), compare it to state-of-the-art AI, and determine how it may aid diagnostics.

Brain-State Transitions, Responsibility, and Personal Identity.

This article examines the emerging possibility of "brain-state transitioning," in which one brain state is prompted through manipulating the dynamics of the active brain. The technique, still in its infancy, is intended to provide the basis for novel treatments for brain-based disorders. Although a detailed literature exists covering topics around brain-machine interfaces, where targets of brain-based activity include artificial limbs, hardware, and software, there is less concentration on the brain itself as a target for instrumental intervention.

Antisense therapy in a rat model of Alexander disease reverses GFAP pathology, white matter deficits, and motor impairment.

Alexander disease (AxD) is a devastating leukodystrophy caused by gain-of-function mutations in , and the only available treatments are supportive. Recent advances in antisense oligonucleotide (ASO) therapy have demonstrated that transcript targeting can be a successful strategy for human neurodegenerative diseases amenable to this approach. We have previously used mouse models of AxD to show that -targeted ASO suppresses protein accumulation and reverses pathology; however, the mice have a mild phenotype with no apparent leukodystrophy or overt clinical features and are therefore limited for assessing functional outcomes.

CSF and Serum Biomarkers of Cerebral Damage in Autoimmune Epilepsy.

Our goal was to investigate whether biomarkers of cerebral damage are found in autoimmune-mediated epilepsy (AIE) and whether these can differentiate AIE from other seizure disorders. We retrospectively searched our cerebrospinal fluid (CSF) database for patients with definite AIE, hippocampal sclerosis due to other causes (HS), genetic generalized epilepsy (GGE), and psychogenic, non-epileptic seizures (PNES). We measured serum and CSF tau, neurofilament 1 (NFL), glial fibrillary acid protein (GFAP), and ubiquitin-carboxy-terminal hydrolase L1 with a single-molecule array.