GLP-1 receptor agonist semaglutide ameliorates motor deficits and tau pathology in the rTg4510s mouse model.

Background: Tauopathies, including Alzheimer's disease, are characterized by progressive neurodegeneration manifesting as motor and cognitive impairments. This study evaluated the therapeutic potential of semaglutide, a clinically approved glucagon-like peptide-1 receptor agonist, in the rTg4510 mouse model of tauopathy.

Methods: Starting at three months of age, rTg4510 mice and wild-type littermates received semaglutide (0.

Combination amide proton transfer imaging with diffusion-weighted imaging for differentiating tumor characteristics and assessing Ki-67 expression in soft tissue tumors.

Purpose: To investigate the utility of amide proton transfer (APT) imaging in conjunction with diffusion-weighted imaging (DWI) for distinguishing between benign and malignant soft tissue tumors (STTs), and to assess the correlation with Ki-67 expression.

Materials And Methods: A retrospective analysis was performed on 67 patients with soft tissue tumors. According to the pathological findings, the cohort was categorized into 39 cases of benign tumors and 28 cases of malignant tumors.

The study on delirium side-effects after ultra-brief pulse electroconvulsive therapy.

Objective: Exploring whether ultra-brief pulse electroconvulsive therapy (ECT) reduces the occurrence of postoperative delirium in patients with schizophrenia (SCZ), and its effects on cholinesterase, inflammatory markers, and hippocampal neural metabolites.

Methods: From August 2022 to August 2023, inpatients at the Affiliated Brain Hospital of Nanjing Medical University diagnosed with SCZ according to the International Statistical Classification of Diseases and Related Health Problems (Tenth Edition ICD-10) and aged 18-55 years were studied. Patients were randomly divided into ultra-brief pulse (UBP) and brief pulse (BP) groups, receiving ultra-brief pulse ECT (pulse width 0.

Adult-onset Rasmussen's encephalitis with anti-AMPA receptor antibodies.

A woman aged 49 years developed focal seizures, with right hemispheric focal slowing on electroencephalograph and right hemisphere focal cortical hyperintensities with subtle atrophy on MR brain scan. Cerebrospinal fluid identified anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor auto-antibodies, but her condition did not respond to immunotherapy for AMPA receptor encephalitis. Subsequent MR brain scan showed striking progressive unihemispheric atrophy, consistent with Rasmussen's encephalitis; she made a good functional recovery with cyclophosphamide.

The homozygous LRRK2.p.N1437D point mutation mouse is a novel model of parkinsonism.

The leucine-rich repeat kinase 2 (LRRK2) gene is one of the most common genetic causes of autosomal dominant Parkinson's disease (PD) and a common genetic risk factor for sporadic PD. However, aged mice with common LRRK2 point mutations fail to exhibit age-related PD-associated behavioral and pathological impairments. We generated a novel mouse model harboring the LRRK2.

Impact of deep brain stimulation on cognitive impairment in Parkinson's disease: A retrospective longitudinal study.

Subthalamic nucleus deep brain stimulation (STN-DBS) is a well-established treatment for improving motor symptoms, non-motor symptoms, and quality of life (QOL) in patients with advanced Parkinson's disease (PD). However, its effects on patients with cognitive impairment (CI) remain controversial due to the unique challenges and risks posed by cognitive decline. This study aimed to evaluate the mid- to long-term impact of STN-DBS on motor function, non-motor symptoms, and QOL in PD patients with CI.

Assessing Plasma APLP1 for the Progression of Parkinson's Disease: Insights from HSPD and PPMI Cohorts.

Background: Amyloid precursor-like protein 1 (APLP1) is involved in pathological α-synuclein transmission, but its role in Parkinson's disease (PD) progression has not been explored.

Objective: This study investigates APLP1 as a potential predictor for motor and cognitive deterioration in PD.

Methods: Plasma APLP1 levels were measured in PD patients from the Huashan Hospital for Parkinson's Disease (HSPD) and Parkinson's Disease Progression Markers Initiative (PPMI) cohorts.

Association of plasma homocysteine with cognitive impairment in patients with Parkinson's disease.

Background: Elevated plasma homocysteine (Hcy) has been reported as a risk factor for cognitive impairment in the general population. However, there are conflicting results regarding the relationship between Hcy and cognitive impairment across various cognitive domains in Parkinson's disease (PD).

Objective: This study aims to explore the association between plasma Hcy levels, cognitive impairment, and dysfunction in various cognitive domains among PD patients with and without mild cognitive impairment (MCI).

In Vivo F-APN-1607 Tau Positron Emission Tomography Imaging in MAPT Mutations: Cross-Sectional and Longitudinal Findings.

Background: Frontotemporal lobar degeneration with tauopathy caused by MAPT (microtubule-associated protein tau) mutations is a highly heterogenous disorder. The ability to visualize and longitudinally monitor tau deposits may be beneficial to understand disease pathophysiology and predict clinical trajectories.

Objective: The aim of this study was to investigate the cross-sectional and longitudinal F-APN-1607 positron emission tomography/computed tomography (PET/CT) imaging findings in MAPT mutation carriers.

Disease progression in Parkinson's disease patients with subjective cognitive complaint.

Objective: Little is known about the disease progression of Parkinson's disease patients with subjective cognitive complaint (PD-SCC). This longitudinal cohort study aims to compare the progression of clinical features and quality of life (QoL) in PD patients with normal cognition (NC), SCC, and mild cognitive impairment (MCI).

Methods: A total of 383 PD patients were enrolled, including 189 PD-NC patients, 59 PD-SCC patients, and 135 PD-MCI patients, with 1-7 years of follow-up.

Neuroprotection of Exendin-4 by Enhanced Autophagy in a Parkinsonian Rat Model of α-Synucleinopathy.

Glucagon-like peptide-1 (GLP-1) receptor stimulation ameliorates parkinsonian motor and non-motor deficits in both experimental animals and patients; however, the disease-modifying mechanisms of GLP-1 receptor activation have remained unknown. The present study investigated whether exendin-4 (a GLP-1 analogue) can rescue motor deficits and exert disease-modifying effects in a parkinsonian rat model of α-synucleinopathy. This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.

Quality of Life in Newly Diagnosed Patients With -Related Parkinson's Disease.

Mutations in the gene are the most common cause of autosomal recessive early-onset Parkinson's disease (PD). However, little is known about the quality of life (QoL) in -related PD. Here, we investigated the patterns of QoL in newly diagnosed -related PD patients.

Propagated α-synucleinopathy recapitulates REM sleep behaviour disorder followed by parkinsonian phenotypes in mice.

Idiopathic rapid eye movement sleep behaviour disorder (RBD) is now recognized as an early manifestation of α-synucleinopathies. Increasing experimental studies demonstrate that manipulative lesion or inactivation of the neurons within the sublaterodorsal tegmental nucleus (also known as the subcoeruleus nucleus in humans) can induce RBD-like behaviours in animals. As current RBD animal models are not established on the basis of α-synucleinopathy, they do not represent the pathological substrate of idiopathic RBD and thus cannot model the phenoconversion to Parkinson's disease.

Disease Progression in Patients with Parkin-Related Parkinson's Disease in a Longitudinal Cohort.

Background: There was a paucity of follow-up studies in the disease progression of early-onset PD patients with Parkin mutations (Parkin-EOPD). Here we conducted a longitudinal study to investigate the progression of motor and cognitive features of Parkin-EOPD patients.

Methods: Genetic analysis was performed via target sequencing and multiplex ligation-dependent probe amplification.

Non-motor Symptoms in Parkinson's Disease Patients with Parkin Mutations: More Depression and Less Executive Dysfunction.

The purpose of this study was to identify differences between genetically undefined (GU) early-onset Parkinson's disease (EOPD) patients and carriers of Parkin mutations on non-motor symptoms (NMSs). EOPD patients (N = 261) underwent targeted sequencing of Parkinson's disease (PD) related genes. Among them, 53 cases carried homozygous or compound heterozygous Parkin mutations (Parkin group) while 208 did not carry known causative PD mutations or risk factors of GBA or Parkin heterozygous mutations (GU group).

Cognitive characteristics in Chinese non-demented PD patients based on gender difference.

Background: Cognitive impairment is one of the non-motor symptoms in Parkinson's disease (PD). In the present study, we aim to examine the cognitive function of non-demented Parkinson's disease patients and compare the results between male and female patients as well as control groups in search of any gender effect.

Methods: Sixty PD Patients (30 males and 30 females) from the Movement Disorders Clinic at Huashan Hospital Affiliated to Fudan University were recruited to participate in the study.

Depressive Symptoms Are Associated With Color Vision but not Olfactory Function in Patients With Parkinson's Disease.

Depressive symptoms and sensory dysfunction, such as reduction in visual and olfactory function, are common in Parkinson's disease (PD). Previous studies have suggested that depressive symptoms are associated with visual impairments and potentially with hyposmia in several types of mood disorders. However, the relationship between depressive symptoms and sensory dysfunction remains unclear in PD.

A homozygous missense variant in HSD17B4 identified in a consanguineous Chinese Han family with type II Perrault syndrome.

Background: Perrault syndrome is a rare multisystem disorder that manifests with sensorineural hearing loss in both sexes, primary ovarian insufficiency in females and neurological features. The syndrome is heterogeneous both genetically and phenotypically.

Case Presentation: We reported a consanguineous family (two affected sisters) with Perrault syndrome.

Fasudil, a Rho kinase inhibitor, promotes the autophagic degradation of A53T α-synuclein by activating the JNK 1/Bcl-2/beclin 1 pathway.

Accumulation of α-synuclein (α-syn) is pivotally implicated in the pathogenesis of Parkinson׳s disease (PD), and enhancing its clearance might be a promising strategy in PD treatment. It has recently been shown that Rho kinase (ROCK) activation is involved in many neurodegenerative diseases, and some ROCK inhibitors might promote the degradation of abnormal protein aggregates. However, it is not known if fasudil, the only ROCK inhibitor available in clinical setting, could promote the degradation of α-syn, and ameliorate the α-syn induced neurotoxicity.