With the increasing clinical use of anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer's disease (AD) in China, some patients have completed or are approaching the predefined treatment period, leading to emerging clinical questions regarding post-treatment maintenance, discontinuation, monitoring, and retreatment. However, no consensus has yet been established on long-term management or sequential-like treatment strategies after anti-Aβ monoclonal antibody therapy. Based on current clinical evidence and the practical experience of the Cognitive Center of Renji Hospital, Shanghai Jiao Tong University School of Medicine, this article proposes an experience-based protocol for sequential-like management of anti-Aβ monoclonal antibody therapy. The protocol uses amyloid PET-derived Centiloid values as the core objective reference and recommends stratified management according to clinical clearance status and prior amyloid clearance rate. After treatment discontinuation, dynamic monitoring with plasma p-tau217 protein and amyloid PET is recommended, and an increase in the Centiloid value to >24.1 CL may serve as an important reference for restarting anti-Aβ monoclonal antibody therapy. This protocol is intended to provide a clinical reference and requires further validation and optimization through real-world studies and long-term follow-up.

Objectives： Parkinson’s disease (PD) is a neurodegenerative disorder affecting multiple systems. Previous studies have indicated that autonomic dysfunction in PD patients may manifest in the early stages of the disease. This study aims to investigate the correlation between autonomic dysfunction and the progression of motor symptoms in PD patients.

Methods： A total of 738 PD patients participated in this research. The status of autonomic dysfunction was examined by Scales for Outcomes in Parkinson's Disease-Autonomic Dysfunction (SCOPA-AUT). And the motor progression was monitored by using Movement Disorder Society-Sponsored Revision of the Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). Besides, neuropsychological status was recorded using Hamilton Depression Scale and Hamilton Anxiety Scale. The participants were followed up for 2 years (±3 months) and the MDS-UPDRS was reassessed to examine the progress in motor function.

Results： The SCOPA-AUT score was significantly correlated with the total MDS-UPDRS score (P＜0.001) as well as the changes in Part Ⅰ (P＝0.005), Part Ⅱ (P＜ 0.001), and Part Ⅲ (P＜0.001) scores (absolute difference between baseline and 2-year follow-up). Among the sub-items of SCOPA-AUT, the scores for autonomic dysfunction related to digestive system, urinary system, cardiovascular symptoms, skin symptoms, and drug use showed significant correlations with the total MDS-UPDRS score and certain sub-scores. However, sexual dysfunction and changes in motor scores did not show significant correlations with the total MDS-UPDRS score or changes in any sub-scores.

Conclusions： Autonomic dysfunction could be considered as a potential predictor of motor progression in PD.

Objective: To report the clinical features of a sporadic amyotrophic lateral sclerosis (ALS) patient carrying a HARS1 variant with mildly elevated cerebrospinal fluid (CSF) protein, and to discuss the clinical significance of CSF protein changes in ALS as well as the co-occurrence of the HARS1 variant and CSF protein elevation.

Methods: The patient's clinical symptoms, electrophysiology, imaging, cerebrospinal fluid, and genetic test results were documented, alongside a literature review and analysis.

Results: The patient, a middle-aged female, presented with a progressively worsening disease course. The primary clinical manifestations included increasing limb weakness, dysarthria, atrophy of the tongue muscles, hyperactive tendon reflexes, and positive pathological signs. Cerebrospinal fluid analysis revealed elevated protein levels. Electromyography demonstrated extensive neurogenic damage, while imaging studies indicated involvement of the corticospinal tract. Genetic testing identified a heterozygous variant of HARS1 c.210G>A (p.Met70Ile).Based on these findings, a clinical diagnosis of ALS was established. Following treatment with riluzole, coenzyme Q10, and short-term corticosteroid therapy, the patient's condition stabilized.

Conclusion: This ALS patient with a rare HARS1 variant suggests a broader clinical spectrum for this gene than previously known. The slight increase in CSF protein indicates blood-brain barrier dysfunction rather than an immune response. The pathogenicity of the HARS1 variant needs further study and additional cases for confirmation. As mild CSF protein elevation is not uncommon in ALS, it should not be interpreted as specifically attributable to the HARS1 variant; the two findings may be independent or indirectly linked by shared neurodegenerative pathology.

Alzheimer’s disease (AD) is a common progressive neurodegenerative disease characterized prominently by recent memory impairment, often accompanied by psychiatric and behavioral symptoms as well as varying degrees of functional impairment in daily living abilities. The insidious onset and gradual progression of AD pose substantial challenges to early clinical diagnosis. Under the amyloid β -tau-neurodegeneration (ATN) diagnostic framework proposed by the National Institute on Aging and Alzheimer’s Association (NIAAA) in 2024, the biological diagnosis of AD mainly relies on cerebrospinal fluid examination and positron emission tomography (PET), but the former is invasive and the latter is expensive and equipment dependent, severely limiting their clinical popularity. Therefore, exploring a non-invasive, economical, and dynamic functional biomarker that can reflect neurodegeneration (i. e., “N”) has become an urgent problem in this field. Electroencephalogram (EEG) has shown unique advantages in the study of cognitive impairment due to its low cost, non-invasive nature, high temporal resolution, and good reproducibility. Its signals are highly sensitive to synaptic dysfunction and abnormal network oscillations, and can capture real-time brain network dysfunction and directly map the electrophysiological basis of neurodegeneration. In recent years, the combined application of EEG with multimodal neuroimaging techniques, such as transcranial magnetic stimulation (TMS), functional magnetic resonance imaging (fMRI), and functional nearinfrared spectroscopy (fNIRS), has developed rapidly, providing rich functional information for early identification of AD from multiple dimensions, including cortical excitability, causal network connectivity, oscillation blood flow coupling, and neurovascular coupling. This article systematically reviews the application progress of resting-state EEG spectrum and microstate analysis, TMS-EEG, EEG-fMRI, and EEG-fNIRS in AD and mild cognitive impairment (MCI), focusing on how these non-invasive techniques complement and integrate with existing ATN diagnostic frameworks. At the same time, it analyzes the limitations faced by current research in sample size, standardization, and clinical translation, and looks forward to future technological optimization, multi-center validation, and potential pathway for intergrating the ATN diagnostic network.

Post-stroke upper-limb motor recovery is often slow, substantially compromising patients' ability to perform activities of daily living and quality of life. As a novel closed-loop neuromodulation strategy, brain-computer interface (BCI) rehabilitation robots can decode neural activity signals in real time and convert them into control commands, enabling information interaction between the brain and the rehabilitation robot. Training with BCI rehabilitation robots can effectively improve upper-limb motor dysfunction in stroke patients. This article systematically reviews the key research progress, neural mechanisms, and existing challenges in the application of BCI rehabilitation robots for upper-limb motor recovery after stroke, aiming to provide references for researchers and clinicians in the fields of rehabilitation medicine, neural engineering, and robotics.