A5022856463- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Dementia and Cognitive Impairment Research
- Parkinson's Disease Mechanisms and Treatments
- Nuclear Receptors and Signaling
- S100 Proteins and Annexins
- Advanced Glycation End Products research
- Tryptophan and brain disorders
- Mitochondrial Function and Pathology
- Neurogenesis and neuroplasticity mechanisms
- Nerve injury and regeneration
- Neurological disorders and treatments
- Immune Response and Inflammation
- Molecular Biology Techniques and Applications
- Neuroscience and Neuropharmacology Research
- RNA Research and Splicing
- Barrier Structure and Function Studies
- Neurological Disorders and Treatments
- Amyotrophic Lateral Sclerosis Research
- Ginkgo biloba and Cashew Applications
- Health, Environment, Cognitive Aging
- Cholinesterase and Neurodegenerative Diseases
- Neonatal and fetal brain pathology
- Drug Transport and Resistance Mechanisms
Banner Sun Health Research Institute
2013-2022
Arizona State University
2016-2020
Arizona Alzheimer’s Consortium
2012-2017
Banner Alzheimer’s Institute
2017
Shiga University of Medical Science
2017
Alzheimer's Association
2012-2017
Barrow Neurological Institute
2017
Shiga University
2017
Banner Health
2001-2009
Columbia University
2004
Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal toxicity in Alzheimer's disease (AD). Here, we demonstrate that Abeta-binding alcohol dehydrogenase (ABAD) direct molecular link from Abeta to mitochondrial toxicity. interacts with ABAD the mitochondria AD patients and transgenic mice. The crystal structure Abeta-bound shows substantial deformation active site prevents nicotinamide adenine dinucleotide (NAD) binding. An peptide specifically inhibits ABAD-Abeta...
The B rain and ody D onation P rogram ( BBDP ) at anner S un H ealth R esearch I nstitute http://www.brainandbodydonationprogram.org started in 1987 with brain‐only donations currently has banked more than 1600 brains. More 430 whole‐body have been received since this service was commenced 2005. collective academic output of the is now described as A rizona tudy ging N eurodegenerative isorders AZSAND ). Most subjects are enrolled cognitively normal volunteers residing retirement communities...
Microglia are critical for amyloid-β peptide (Aβ)-mediated neuronal perturbation relevant to Alzheimer's disease (AD) pathogenesis. We demonstrate that overexpression of receptor advanced glycation end products (RAGE) in imbroglio exaggerates neuroinflammation, as evidenced by increased proinflammatory mediator production, Aβ accumulation, impaired learning/memory, and neurotoxicity an Aβ-rich environment. Transgenic (Tg) mice expressing human mutant APP (mAPP) neurons RAGE microglia...
Mitochondrial dysfunction and synaptic damage are early pathological features of the Alzheimer's disease-affected brain. Memory impairment in disease is a manifestation brain pathologies such as accumulation amyloid-β peptide mitochondrial damage. The underlying pathogenic mechanisms effective disease-modifying therapies for remain elusive. Here, we demonstrate first time that decreased PTEN-induced putative kinase 1 (PINK1) expression associated with pathology. Restoring neuronal PINK1...
Abstract We have previously developed and characterized isolated microglia astrocyte cultures from rapid (<4 h) brain autopsies of Alzheimer's disease (AD) nondemented elderly control (ND) patients. In the present study, we evaluate inflammatory repertoire AD ND cultured white matter (corpus callosum) gray (superior frontal gyrus) with respect to three major proinflammatory cytokines, chemokines, a classical pathway complement component, scavenger cell growth factor, reactive nitrogen...
The Brain Donation Program at Sun Health Research Institute has been in continual operation since 1987, with over 1000 brains banked. population studied primarily resides the retirement communities of northwest metropolitan Phoenix, Arizona. is affiliated Health, a nonprofit community-owned and operated health care provider. Subjects are enrolled prospectively to allow standardized clinical assessments during life. Funding comes from competitive grants. made short postmortem brain retrieval...
We evaluated entorhinal cortex and superior frontal gyrus for hallmarks of Alzheimer's disease (AD) pathology, including inflammation, in three patient sets: AD patients, nondemented elderly patients with few or no neurofibrillary tangles (NFTs) amyloid β peptide (Aβ) deposits, i.e. normal controls (NC), profuse NFTs neocortical Aβ high pathology (HPC). Membrane attack complex (C5b-9) immunoreactivity immune activation microglia (MHCII expression) were used as general markers inflammation....
Alzheimer's disease (AD) is characterized by accumulation and deposition of Abeta peptides in the brain. cerebrovessels occurs many AD patients results cerebral amyloid angiopathy (AD/CAA). Since can be transported across blood-brain barrier (BBB), aberrant trafficking BBB may contribute to brain CAA development. Expression analyses 273 BBB-related genes performed this study showed that drug transporter, ABCG2, was significantly upregulated brains AD/CAA compared with age-matched controls....
Abstract Triggering receptor expressed by myeloid cells 2 ( TREM 2), a member of the immunoglobulin superfamily, has anti‐inflammatory phagocytic function in cells. Several studies have shown that gene variant rs75932628‐ T increased risks for A lzheimer's disease AD ), P arkinson's disease, frontotemporal dementia and amyotrophic lateral sclerosis. It been suggested could be resulted from loss caused mutation. Indeed, new evidence showed several mutations immunoglobulin‐like V ‐region led...
Neuroinflammation is considered a key pathological process in neurodegenerative diseases of aging, including Alzheimer's disease (AD). Many studies have defined phenotypes reactive microglia, the brain-resident macrophages, with different antigenic markers to identify those potentially causing inflammatory damage. We took an alternative approach goal characterizing distribution purinergic receptor P2RY12-positive marker previously as identifying homeostatic or non-activated microglia....
The utility of plasma amyloid beta (Aβ) and tau levels for the clinical diagnosis Alzheimer's disease (AD) dementia has been controversial. main objective this study was to compare Aβ42 measured by ultra-sensitive immunomagnetic reduction (IMR) assays in samples collected at Banner Sun Health Institute (BSHRI) (United States) with those from National Taiwan University Hospital (NTUH) (Taiwan). Significant increase were detected AD subjects both cohorts, while increased only NTUH cohort. A...