A5060656369- Alzheimer's disease research and treatments
- Prion Diseases and Protein Misfolding
- Dementia and Cognitive Impairment Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Computational Drug Discovery Methods
- Trace Elements in Health
- Neuroscience and Neuropharmacology Research
- Advanced Neuroimaging Techniques and Applications
- Neurological Disease Mechanisms and Treatments
- Tryptophan and brain disorders
- S100 Proteins and Annexins
- Bioinformatics and Genomic Networks
- Neurological diseases and metabolism
- Functional Brain Connectivity Studies
- Mitochondrial Function and Pathology
- Intracerebral and Subarachnoid Hemorrhage Research
- Autism Spectrum Disorder Research
- Long-Term Effects of COVID-19
- Parkinson's Disease Mechanisms and Treatments
- Down syndrome and intellectual disability research
- Advanced MRI Techniques and Applications
- Intensive Care Unit Cognitive Disorders
- Nuclear Receptors and Signaling
New York University
2016-2025
New York State Office for People With Developmental Disabilities
1992-2024
University of Gothenburg
2012-2024
NYU Langone Health
2015-2024
University School
2001-2024
Center for Neuro-Oncology
2016-2024
Alzheimer’s Disease Neuroimaging Initiative
2023-2024
Cornell University
2024
Weill Cornell Medicine
2024
Montefiore Medical Center
2024
Many biochemically diverse proteins can give rise to amyloid fibrils; however, they are all accompanied by P component and glucosaminoglycans. With antibodies specific apolipoprotein E (apo E) we used immunohistochemical techniques test for the presence of this protein in both cerebral systemic amyloid. We found apo immunoreactivity tested types In deposits P, glucosaminoglycans may be acting as ‘pathological molecular chaperones’. The latter define a group unrelated that induce β-pleated...
Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid β-protein (Aβ) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage thus expression the β-amyloid precursor protein. Because neuropathological phenotype in older DS subjects closely resembles that AD, examination brains increasing age provides a unique model progression AD. Here, we characterized deposition several Aβ peptides apolipoprotein E formalin-fixed brain...
Autism is characterized by a broad spectrum of clinical manifestations including qualitative impairments in social interactions and communication, repetitive stereotyped patterns behavior. Abnormal acceleration brain growth early childhood, signs slower neurons, minicolumn developmental abnormalities suggest multiregional alterations. The aim this study was to detect the focal defects identify regions that are prone alterations autism. Formalin-fixed hemispheres 13 autistic (4–60 years age)...
Late-onset and sporadic Alzheimer's disease are associated with the apolipoprotein E (apoE) type 4 allele expressing protein isoform apoE4. Apolipoprotein binds avidly to beta amyloid (A beta) peptide, a major component of senile plaque disease, in an isoform-specific manner. The apoE4 A peptide more rapidly than apoE3. We observed that soluble SDS-stable complexes apoE3 or apoE4, formed by coincubation precipitated after several days incubation at 37 degrees C precipitating complexes....
The current development of immunotherapy for Alzheimer's disease is based on the assumption that human-derived amyloid beta protein (Abeta) can be targeted in a similar manner to animal cell-derived or synthetic Abeta. Because structure Abeta depends its source and presence cofactors, it great interest determine whether oligomeric species impair brain function and, if so, not their disruptive effects prevented using antibodies. We report untreated ex vivo human CSF contains dimers rapidly...
Abstract Objective To report a novel prion disease characterized by distinct histopathological and immunostaining features, associated with an abnormal isoform of the protein (PrP) that, contrary to common diseases, is predominantly sensitive protease digestion. Methods Eleven subjects were investigated at National Prion Disease Pathology Surveillance Center for clinical, histopathological, immunohistochemical, genotypical, PrP characteristics. Results Patients presented behavioral...
To determine the prevalence and associated mortality of well-defined neurologic diagnoses among patients with coronavirus disease 2019 (COVID-19), we prospectively followed hospitalized severe acute respiratory syndrome 2 (SARS-CoV-2)-positive recorded new disorders hospital outcomes.
In the United States, estimates indicate there are between 250,000 and 400,000 individuals with Down syndrome (DS), nearly all will develop Alzheimer's disease (AD) pathology starting in their 30s. With current lifespan being 55 to 60 years, approximately 70% dementia, if life expectancy continues increase, number of developing AD concomitantly increase. Pathogenic mechanistic links DS prompted Association partner Linda Crnic Institute for Syndrome Global Foundation at a workshop experts...
Accumulation of phosphorylated tau is a key pathological feature Alzheimer's disease. Phosphorylated accumulation causes synaptic impairment, neuronal dysfunction and formation neurofibrillary tangles. The actions are mediated by surrounding proteins; however, comprehensive understanding the proteins that interacts with in disease surprisingly limited. Therefore, aim this study was to determine interactome. To end, we used two complementary proteomics approaches: (i) quantitative performed...
Aggregation of amyloid β-peptide (Aβ) is implicated in the pathology Alzheimer's disease (AD), with soluble, Aβ oligomeric species thought to be critical pathological species. Identification and characterization intermediate formed during aggregation process crucial understanding mechanisms by which mediate neuronal toxicity following progression. Probing these proved extremely challenging, as evident lack reliable sensors, due their heterogeneous transient nature. We describe here an...
Abstract Introduction Neurological complications among hospitalized COVID‐19 patients may be associated with elevated neurodegenerative biomarkers. Methods Among without a history of dementia (N = 251), we compared serum total tau (t‐tau), phosphorylated tau‐181 (p‐tau181), glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), ubiquitin carboxy‐terminal hydrolase L1 (UCHL1), and amyloid beta (Aβ40,42) between or encephalopathy, in‐hospital death versus survival, discharge...