Lon S. Schneider
A5103077621- Dementia and Cognitive Impairment Research
- Alzheimer's disease research and treatments
- Cholinesterase and Neurodegenerative Diseases
- Functional Brain Connectivity Studies
- Schizophrenia research and treatment
- Health Systems, Economic Evaluations, Quality of Life
- Neurological Disease Mechanisms and Treatments
- Computational Drug Discovery Methods
- Treatment of Major Depression
- Diet and metabolism studies
- Health, Environment, Cognitive Aging
- Parkinson's Disease Mechanisms and Treatments
- Bioinformatics and Genomic Networks
- Genetic Associations and Epidemiology
- Pharmaceutical Practices and Patient Outcomes
- Ginkgo biloba and Cashew Applications
- Advanced Neuroimaging Techniques and Applications
- Neurological Disorders and Treatments
- Folate and B Vitamins Research
- Attention Deficit Hyperactivity Disorder
- Bipolar Disorder and Treatment
- Estrogen and related hormone effects
- Memory and Neural Mechanisms
- Menopause: Health Impacts and Treatments
- Blood Pressure and Hypertension Studies
University of Southern California
2016-2025
Keck Hospital of USC
2015-2024
Alzheimer’s Disease Neuroimaging Initiative
2023-2024
LAC+USC Medical Center
2016-2022
Laboratoire d’Imagerie Biomédicale
2022
Alzheimer Precision Medicine
2022
Inserm
2022
Centre National de la Recherche Scientifique
2022
Southern States University
2020
Avraham Pharmaceuticals (Israel)
2019
There is evidence that medications or vitamins increase the levels of brain catecholamines and protect against oxidative damage may reduce neuronal slow progression Alzheimer's disease.
Abstract Multifactorial mechanisms underlying late-onset Alzheimer’s disease (LOAD) are poorly characterized from an integrative perspective. Here spatiotemporal alterations in brain amyloid-β deposition, metabolism, vascular, functional activity at rest, structural properties, cognitive integrity and peripheral proteins levels relation to LOAD progression. We analyse over 7,700 images tens of plasma cerebrospinal fluid biomarkers the Disease Neuroimaging Initiative (ADNI). Through a...
In Alzheimer's disease, there is a marked decline in the function of cholinergic neurons brain. However, studies treatment with cholinesterase inhibitors have produced conflicting results. We conducted multicenter trial to evaluate whether inhibitor tacrine (1,2,3,4-tetrahydro-9-acridinamine monohydrochloride monohydrate) could improve cognition patients disease.
Abstract Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging–Alzheimer's Association describes biomarker‐based pathologic definition of focused amyloid, tau, neuronal injury. In response this article, here we first discussed that dysfunction is an important early event in...
Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia contribute to pathophysiology by vascular direct neurotoxic mechanisms. Even the absence vitamin deficiency, can reduced administration high-dose supplements folic acid vitamins B(6) B(12). Prior studies B reduce AD have not had sufficient size or duration assess their effect on cognitive decline.To determine efficacy safety supplementation treatment AD.A multicenter, randomized, double-blind...
Abstract Alzheimer's disease and related dementias (ADRDs) are a global crisis facing the aging population society as whole. With numbers of people with ADRDs predicted to rise dramatically across world, scientific community can no longer neglect need for research focusing on among underrepresented ethnoracial diverse groups. The Association International Society Advance Research Treatment (ISTAART; alz.org/ISTAART ) comprises number professional interest areas (PIAs), each major area...
Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to through neuronal connections, facilitated by β-amyloid (Aβ). We test this hypothesis in humans using an epidemic spreading model (ESM) simulate spread, compare these simulations observed patterns measured tau-PET 312 individuals along disease continuum. Up 70% the variance overall spatial pattern can be explained our model. Surprisingly, ESM predicts irrespective whether brain...
Abstract Alzheimer’s disease (AD) is a progressive neurodegenerative condition marked by decline in cognitive functions with no validated modifying treatment. It critical for timely treatment to detect AD its earlier stage before clinical manifestation. Mild impairment (MCI) an intermediate between cognitively normal older adults and AD. To predict conversion from MCI probable AD, we applied deep learning approach, multimodal recurrent neural network. We developed integrative framework that...
Objective: The study measured the effects of atypical antipsychotics on psychiatric and behavioral symptoms in patients with Alzheimer’s disease psychosis or agitated behavior. Method: Clinical Antipsychotic Trials Intervention Effectiveness—Alzheimer’s Disease (CATIE-AD) effectiveness included 421 outpatients agitated/aggressive Patients were assigned randomly to masked, flexible-dose treatment olanzapine, quetiapine, risperidone, placebo for up 36 weeks. could be reassigned a different...
To estimate a regional progression pattern of amyloid deposition from cross-sectional amyloid-sensitive PET data and evaluate its potential for in vivo staging an individual's pathology.
Objective: The impact of the atypical antipsychotics olanzapine, quetiapine, and risperidone on cognition in patients with Alzheimer's disease is unclear. authors assessed effects time treatment neuropsychological functioning during Clinical Antipsychotic Trials Intervention Effectiveness–Alzheimer's Disease study (CATIE-AD). Method: CATIE-AD included 421 outpatients psychosis or agitated/aggressive behavior who were randomly assigned to receive masked, flexible-dose risperidone, placebo....
BackgroundBrain amyloidosis does not invariably predict dementia. We hypothesized that high soluble 42-amino acid β amyloid (Aβ42) peptide levels are associated with normal cognition and hippocampal volume despite increasing brain amyloidosis.MethodsThis cross-sectional study of 598 amyloid-positive participants in the Alzheimer's Disease Neuroimaging Initiative cohort examined whether Aβ42 higher (NC) individuals compared to mild cognitive impairment (MCI) disease (AD) this relationship...
<h3>Importance</h3> Late-life depression (LLD) is characterized by considerable heterogeneity in clinical manifestation. Unraveling such might aid elucidating etiological mechanisms and support precision individualized medicine. <h3>Objective</h3> To cross-sectionally longitudinally delineate disease-related LLD associated with neuroanatomy, cognitive functioning, symptoms, genetic profiles. <h3>Design, Setting, Participants</h3> The Imaging-Based Coordinate System for Aging...
Abstract For optimal design of anti-amyloid-β (Aβ) and anti-tau clinical trials, we need to better understand the pathophysiological cascade Aβ- tau-related processes. Therefore, set out investigate how Aβ soluble phosphorylated tau (p-tau) relate accumulation aggregates assessed with PET subsequent cognitive decline across Alzheimer’s disease (AD) continuum. Using human cross-sectional longitudinal neuroimaging assessment data, show that in early stages AD, increased concentration CSF p-tau...
<b><i>Background:</i></b> Treatment of agitation is a crucial problem in the care patients with AD. Although antipsychotic and antidepressant medications behavior management techniques (BMT) have each been used to treat agitation, clinical trials these treatments characterized by small sample sizes uncontrolled treatment designs. <b><i>Objective:</i></b> To compare haloperidol, trazodone, BMT placebo AD outpatients. <b><i>Methods:</i></b> A total 149 their caregivers participated randomized,...
<b>Objective: </b> To examine whether estrogen replacement therapy (ERT) affects clinical and cognitive responses to tacrine in women with Alzheimer9s disease (AD). Design: A 30-week, randomized, double-blind, placebo-controlled, parallel-group, multicenter trial of which a subgroup were receiving ERT prior randomization. Patients: Women mild moderate-stage AD, at least 50 years age, who enrolled the previously reported trial. Interventions: Randomized assignment placebo or one three...
Regions of the temporal and parietal lobes are particularly damaged in Alzheimer's disease (AD), this leads to a predictable pattern brain atrophy. In vivo quantification subregional atrophy, such as changes cortical thickness or structure volume, could lead improved diagnosis better assessment neuroprotective effects therapy. Toward end, we have developed fast robust method for accurately quantifying cerebral structural several subcortical regions using serial MRI scans. 169 healthy...
To identify clinical predictors of cognitive decline in Alzheimer's disease.A cohort patients was followed up longitudinally and the likelihood arriving at two end points assessed using Cox proportional hazards model eight explanatory variables.Subjects were chosen from examined for memory loss medical centers affiliated with University Southern California, Los Angeles.The sample included 135 who met National Institute Neurological Communicative Disorders Stroke-Alzheimer's Disease Related...