A5035899769- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Prion Diseases and Protein Misfolding
- Cholinesterase and Neurodegenerative Diseases
- Computational Drug Discovery Methods
- Trace Elements in Health
- Monoclonal and Polyclonal Antibodies Research
- Tryptophan and brain disorders
- Advanced Neuroimaging Techniques and Applications
- Drug Transport and Resistance Mechanisms
- 14-3-3 protein interactions
- Nuclear Receptors and Signaling
- Glycosylation and Glycoproteins Research
- Neurological Disease Mechanisms and Treatments
- Machine Learning in Bioinformatics
- Cellular transport and secretion
- S100 Proteins and Annexins
- Dementia and Cognitive Impairment Research
- Advanced Biosensing Techniques and Applications
- Nicotinic Acetylcholine Receptors Study
- RNA Interference and Gene Delivery
- Autophagy in Disease and Therapy
- Advanced MRI Techniques and Applications
- Memory and Neural Mechanisms
New York University
2016-2025
NYU Langone Health
2010-2024
Neuroscience Institute
2024
Neurosciences Institute
2018-2019
University of Iceland
2012
University School
2005
Health First
2004
Columbia University Irving Medical Center
1998-2003
University Medical Center
2002
Loyola University Medical Center
1995-1997
Immunotherapies for various neurodegenerative diseases have recently emerged as a promising approach clearing pathological protein conformers in these disorders. This type of treatment has not been assessed models that develop neuronal tau aggregates observed frontotemporal dementia and Alzheimer's disease. Here, we present active immunization with phosphorylated epitope, P301L tangle model mice, reduces aggregated the brain slows progression tangle-related behavioral phenotype. Females had...
Targeting hyperphosphorylated tau by immunotherapy is emerging as a promising approach to treat tauopathies such Alzheimer's disease and frontotemporal dementia. We have previously reported that active immunization clears aggregates from the brain attenuates or prevents functional impairments in two different tangle mouse models. Here, we assessed efficacy of passive with PHF1 antibody, which targets phospho-epitope within one our immunogens. Homozygous female mice (JNPL3, 2-3 months) were...
Harnessing the immune system to clear protein aggregates is emerging as a promising approach treat various neurodegenerative diseases. In Alzheimer's disease (AD), several clinical trials are ongoing using active and passive immunotherapy targeting amyloid-β (Aβ) peptide. Limited emphasis has been put into clearing tau/tangle pathology, another major hallmark of disease. Recent findings from first Aβ vaccination trial suggest that this limited effect on tau pathology plaque clearance may not...
Abstract Non-fibrillar soluble oligomeric forms of amyloid-β peptide (oAβ) and tau proteins are likely to play a major role in Alzheimer’s disease (AD). The prevailing hypothesis on the etiopathogenesis is that oAβ initiates pathology slowly spreads throughout medial temporal cortex neocortices independently Aβ, eventually leading memory loss. Here we show brief exposure extracellular recombinant human oligomers (oTau), but not monomers, produces an impairment long-term potentiation (LTP)...
Abstract The presence of amyloid‐β (Aβ) plaques in the brain is a hallmark pathological feature Alzheimer's disease (AD). Transgenic mice overexpressing mutant amyloid precursor protein (APP), or both APP and presenilin‐1 (APP/PS1), develop Aβ similar to those AD patients, have been proposed as animal models which test experimental therapeutic approaches for clearance Aβ. However, at present there no vivo whole‐brain imaging method detect men. A novel presented brains transgenic by magnetic...
Abstract Background Tau is a microtubule stabilizing protein and mainly expressed in neurons. aggregation into oligomers tangles considered an important pathological event tauopathies, such as frontotemporal dementia (FTD) Alzheimer’s disease (AD). Tauopathies are also associated with deficits synaptic plasticity long-term potentiation (LTP), but the specific role of tau manifestation these deficiencies not well-understood. We examined long lasting forms JNPL3 (BL6) mice expressing mutant...
The prion protein (PrP) binds copper and under some conditions can facilitate its folding into a more protease resistant form. Hence, levels may influence the infectivity of scrapie form (PrPSc). To determine feasibility copper-targeted therapy for disease, we treated mice with chelator, d-(–)-penicillamine (d-PEN), starting immediately following intraperitoneal inoculation. d-PEN delayed onset disease in by about 11 days (p = 0.002), reduced brain 29% < 0.01) blood 22% 0.03) compared...
Immunization with amyloid-beta (Abeta) 1-42 has been shown to reduce amyloid burden and improve cognition in Alzheimer's disease (AD) model mice. In a human trial, possible cognitive benefit was found but association significant toxicity minority of patients. We proposed that immunization nonfibrillogenic Abeta derivatives is much less likely produce have previously one such derivative (K6Abeta1-30) can mice similar extent as Abeta1-42. Here, we immunized AD (Tg2576) Abeta1-30[E18E19] or...
Abstract Memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist, has been shown to improve learning and memory in several preclinical models of Alzheimer's disease (AD). Memantine also reduce the levels amyloid β (Aβ) peptides human neuroblastoma cells as well inhibit Aβ oligomer‐induced synaptic loss. In this study, we assessed whether NMDA inhibition by memantine transgenic mice expressing amyloid‐beta precursor protein (APP) presenilin 1 (PS1) is associated with cognitive benefit...