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Kiren Ubhi

Researcher at University of California, San Diego

Publications -  39
Citations -  2593

Kiren Ubhi is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Alpha-synuclein & Neurotrophic factors. The author has an hindex of 24, co-authored 39 publications receiving 2295 citations. Previous affiliations of Kiren Ubhi include University of California, Berkeley.

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Passive Immunization Reduces Behavioral and Neuropathological Deficits in an Alpha-Synuclein Transgenic Model of Lewy Body Disease

TL;DR: 9E4 was effective at reducing behavioral deficits in the water maze and immunization with 9E4 reduced the accumulation of calpain-cleaved α-syn in axons and synapses and the associated neurodegenerative deficits, suggesting that passive immunizations with monoclonal antibodies may be of therapeutic relevance in patients with PD and DLB.
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Reducing C-terminal-truncated alpha-synuclein by immunotherapy attenuates neurodegeneration and propagation in Parkinson's disease-like models.

TL;DR: It is demonstrated that antibodies against the CT of α-syn reduce levels of CT-truncated fragments of the protein and its propagation, thus ameliorating PD-like pathology and improving behavioral and motor functions in a mouse model of this disease.
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Progressive accumulation of amyloid‐β oligomers in Alzheimer’s disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins

TL;DR: In this article, postmortem frontal cortex samples from controls and patients with Alzheimer's disease were fractionated and analyzed for levels of oligomers and synaptic proteins, and the strongest associations were found with amyloid-beta dimers and pentamers.
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Neurodegeneration in a Transgenic Mouse Model of Multiple System Atrophy Is Associated with Altered Expression of Oligodendroglial-Derived Neurotrophic Factors

TL;DR: Analysis of GDNF expression levels in human MSA samples demonstrated a decrease in the white frontal cortex and to a lesser degree in the cerebellum compared with controls, suggesting a mechanism in which αsyn expression in oligodendrocytes impacts on the trophic support provided by these cells for neurons, perhaps contributing to neurodegeneration.