Publications by authors named "Binyin Li"

Introduction: To investigate the associations of metabotropic glutamate receptor 5 (mGluR5) with tau deposition and cognitive ability in patients with early Alzheimer's disease (AD).

Methods: Twenty-six cognitively impaired (CI) and 14 cognitively unimpaired (CU) individuals underwent mGluR5 positron emission tomography (PET) ([F]PSS232), amyloid PET ([F]florbetapir), and tau PET ([F]MK6240), and neuropsychological assessment. The relationships among mGluR5 availability, tau deposition, and neuropsychological assessment were analyzed using Spearman's correlation and mediation analyses.

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Background Synaptic loss is an important factor in Alzheimer disease (AD); however, blood assays that conveniently and rapidly reflect changes in synaptic density are lacking. Purpose To correlate multiple potential synaptic blood markers with synaptic density measured using F-SynVesT-1, a fluorine 18 (F)-labeled radiotracer, brain PET and to explore the independent associations between these markers and synaptic density. Materials and Methods This prospective study included 50 cognitively unimpaired (mean age, 65.

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Article Synopsis
  • The nucleus basalis of Meynert (NBM) is crucial for understanding Alzheimer's Disease (AD) and its impact on the cholinergic system, yet the link between synaptic loss in the NBM and AD symptoms remains unclear.
  • A study involving 120 participants, including cognitively normal controls and those with cognitive impairment, used MRI and PET imaging to analyze synaptic density in the NBM and its correlation with cognitive performance and traditional AD biomarkers.
  • Findings revealed that lower synaptic density in the NBM was strongly associated with worse cognitive function and neurodegeneration, suggesting that neurite density in related white matter tracts may mediate this relationship.
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Introduction: We investigated the association between white matter hyperintensities (WMH) and regional cortical thickness, amyloid and tau deposition, and synaptic density in the WMH-connected cortex using multimodal images.

Methods: We included 107 participants (59 with Alzheimer's disease [AD]; 27 with mild cognitive impairment; 21 cognitively normal controls) with amyloid beta (Aβ) positivity on amyloid positron emission tomography (PET). The cortex connected to WMH was identified using probabilistic tractography.

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The associations of synaptic loss with amyloid-β (Aβ) and tau pathology measured by positron emission tomography (PET) and plasma analysis in Alzheimer's disease (AD) patients are unknown. Seventy-five participants, including 26 AD patients, 19 mild cognitive impairment (MCI) patients, and 30 normal controls (NCs), underwent [F]SynVesT-1 PET/MR scans to assess synaptic density and [F]florbetapir and [F]MK6240 PET/CT scans to evaluate Aβ plaques and tau tangles. Among them, 19 AD patients, 12 MCI patients, and 29 NCs had plasma Aβ42/40 and p-tau181 levels measured by the Simoa platform.

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Introduction: We aimed to investigate the effect of apolipoprotein E4 (APOE) ε4 on synaptic density in cognitively impaired (CI) participants.

Methods: One hundred ten CI participants underwent amyloid positron emission tomography (PET) with F-florbetapir and synaptic density PET with F-SynVesT-1. We evaluated the influence of APOE ε4 allele on synaptic density and investigated the effects of ε4 genotype on the associations of synaptic density with Alzheimer's disease (AD) biomarkers.

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Recent efforts demonstrated the efficacy of identifying early-stage neuropathology of Alzheimer's disease (AD) through lumbar puncture cerebrospinal fluid assessment and positron emission tomography (PET) radiotracer imaging. These methods are effective yet are invasive, expensive, and not widely accessible. We extend and improve the multiscale structural mapping (MSSM) procedure to develop structural indicators of β-amyloid neuropathology in preclinical AD, by capturing both macrostructural and microstructural properties throughout the cerebral cortex using a structural MRI.

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Background: Tai Chi was found to improve motor symptoms in Parkinson's disease (PD). Whether long-term Tai Chi training could improve non-motor symptoms (NMS) and the related mechanisms were unknown.

Objective: To investigate Tai Chi's impact on non-motor symptoms in PD and related mechanisms.

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Background: Alzheimer's disease (AD) is a multi-gene inherited disease, and apolipoprotein E () ɛ4 is a strong risk factor. Other genetic factors are important but limited.

Objective: This study aimed to investigate the relationship between 17 single-nucleotide polymorphisms (SNPs) and AD in the Southern Chinese populations.

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Cortical gray to white matter signal intensity ratio (GWR) measured from T1-weighted magnetic resonance (MR) images was associated with neurodegeneration and dementia. We characterized topological patterns of GWR during AD pathogenesis and investigated its association with cognitive decline. The study included a cross-sectional dataset and a longitudinal dataset.

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Article Synopsis
  • Amyloid deposition is a key factor in Alzheimer's disease, and this study investigates its prevalence and related risk factors among AD patients in Chinese cities, focusing on urban communities and memory clinics.
  • A total of 1,026 participants were analyzed, revealing high amyloid-positive rates in individuals with clinically diagnosed Alzheimer's (85.8%) and mild cognitive impairment (44.5%), with various factors like age and ApoE ε4 influencing amyloid pathology.
  • The findings suggest that risk factors for amyloid pathology differ across cognitive statuses, highlighting the role of education in mild cognitive impairment and the influence of gender and age in normal cognition.
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Aims: To compare the fecal levels of short-chain fatty acids (SCFAs) in patients with mild cognitive impairment (MCI) and normal controls (NCs) and to examine whether fecal SCFAs could be used as the biomarker for the identification of patients with MCI. To examine the relationship between fecal SCFAs and amyloid-β (Aβ) deposition in the brain.

Methods: A cohort of 32 MCI patients, 23 Parkinson's disease (PD) patients, and 27 NC were recruited in our study.

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Synapse loss has been considered as a major pathological change in Alzheimer's disease (AD). It remains unclear about whether and how synapse loss relates to functional and structural connectivity dysfunction in AD. We measured synaptic vesicle glycoprotein 2 A (SV2A) binding using F-SynVesT-1 PET to evaluate synaptic alterations in 33 participants with AD, 31 with mild cognitive impairment (MCI), and 30 controls.

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Background: The relationship between switching rate of multilayer functional network and cognitive ability in mild cognitive impairment (MCI) and Alzheimers' disease remains unclear.

Methods: We followed up MCI patients for one year and analyzed the association of switching rates with cognitive decline. The iterative and ordinal Louvain algorithm tracked the switching of functional networks, while elastic network regression and Bayesian belief networks were used to test the relationship between network switching rate and cognitive performance cross-sectionally and longitudinally.

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  • Parkinson's disease (PD) is a movement disorder marked by the loss of dopamine-producing pathways, leading to changes in motor coordination and a proposed three-stage progression from silent onset to clinical symptoms.
  • Recent research utilized advanced imaging techniques to observe structural changes in the motor cortex and corticospinal tract in patients with PD, revealing adaptive alterations linked to the disease's progression.
  • Findings indicate that while there is no neuron loss in the motor cortex during early or late PD stages, significant changes occur in axonal structure and myelination, along with markers of neurodegeneration, highlighting early impacts of PD on motor networks.
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Mushroom spine loss and calcium dyshomeostasis are early hallmark events of age-related neurodegeneration, such as Alzheimer's disease (AD), that are connected with neuronal hyperactivity in early pathology of cognitive brain areas. However, it remains elusive how these key events are triggered at the molecular level for the neuronal abnormality that occurs at the initial stage of disease. Here, we identify downregulated miR-339-5p and its upregulated target protein, neuronatin (Nnat), in cortex neurons from the presenilin-1 M146V knockin (PSEN1-M146V KI) mouse model of familial AD (FAD).

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CSF1R-related leukoencephalopathy is an adult-onset white matter disease with high disability and mortality, while little is known about its pathogenesis. This study introduced amplitude of low-frequency fluctuations (ALFF) and regional homogeneity (ReHo) based on resting-state functional magnetic resonance imaging(rsfMRI) to compare the spontaneous brain activities of patients and healthy controls, aiming to enhance our understanding of the disease. RsfMRI was performed on 16 patients and 23 healthy controls, and preprocessed for calculation of ALFF and ReHo.

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Introduction: Cognitive training and physical exercise have shown positive effects on delaying progression of mild cognitive impairment (MCI) to dementia.

Methods: We explored the enhancing effect from Tai Chi when it was provided with cognitive training for MCI. In the first 12 months, the cognitive training group (CT) had cognitive training, and the mixed group (MixT) had additional Tai Chi training.

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The aberrant organization and functioning of three core neurocognitive networks (NCNs), i.e., default-mode network (DMN), central executive network (CEN), and salience network (SN), are among the prominent features in Alzheimer's disease (AD).

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Background: Tai Chi has been shown to improve motor symptoms in Parkinson's disease (PD), but its long-term effects and the related mechanisms remain to be elucidated. In this study, we investigated the effects of long-term Tai Chi training on motor symptoms in PD and the underlying mechanisms.

Methods: Ninety-five early-stage PD patients were enrolled and randomly divided into Tai Chi (n = 32), brisk walking (n = 31) and no-exercise (n = 32) groups.

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The recently described biological framework of Alzheimer's disease (AD) emphasizes three types of pathology to characterize this disorder, referred to as the 'amyloid/tau/neurodegeneration' (A-T-N) status. The 'neurodegenerative' component is typically defined by atrophy measures derived from structural magnetic resonance imaging (MRI) such as hippocampal volume. Neurodegeneration measures from imaging are associated with disease symptoms and prognosis.

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