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Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders.
TLDR
Results suggest that accumulation of wild-type alpha-synuclein may play a causal role in Parkinson's disease and related conditions.
Differential neuropathological alterations in transgenic mice expressing α‐synuclein from the platelet‐derived growth factor and Thy‐1 promoters
TLDR
Comparisons of patterns of human α‐synuclein accumulation in the brains of transgenic mice expressing this molecule from the murine Thy‐1 and platelet‐derived growth factor (PDGF) promoters show a more widespread accumulation of this protein in transgenic mouse brains.
alpha-synuclein promotes mitochondrial deficit and oxidative stress.
TLDR
Results suggest that abnormal accumulation of alpha-synuclein could lead to mitochondrial alterations that may result in oxidative stress and, eventually, cell death.
beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease.
TLDR
Treatments that block the production or accumulation of beta-amyloid peptides could benefit a broader spectrum of disorders than previously anticipated, including Alzheimer's disease and Parkinson's disease.
β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease
TLDR
Treatments that block the production or accumulation of β-amyloid peptides could benefit a broader spectrum of disorders than previously anticipated.
α-Synuclein Protects against Oxidative Stress via Inactivation of the c-Jun N-terminal Kinase Stress-signaling Pathway in Neuronal Cells*
TLDR
Results suggest that increased α-synuclein expression might protect cells from oxidative stress by inactivation of JNK via increased expression of JIP-1b/IB1, which may play a mutual role in the neuronal response to injury and neurodegeneration.
Stress induced morphological microglial activation in the rodent brain: Involvement of interleukin-18
TLDR
Evidence is reported that physical/emotional stress may induce morphological microglial activation in the brain and this activation is in part mediated by interleukin-18.
Effects of alpha-synuclein immunization in a mouse model of Parkinson's disease.
TLDR
It is suggested that vaccination is effective in reducing neuronal accumulation of halpha-syn aggregates and that further development of this approach might have a potential role in the treatment of LBD.
Neurological and Neurodegenerative Alterations in a Transgenic Mouse Model Expressing Human α-Synuclein under Oligodendrocyte Promoter: Implications for Multiple System Atrophy
TLDR
The contention that accumulation of α-syn in oligodendrocytes promotes neurodegeneration and recapitulates several of the key functional and neuropathological features of MSA is supported.
α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress
TLDR
Results suggest that abnormal accumulation of α-synuclein could lead to mitochondrial alterations that may result in oxidative stress and, eventually, cell death.
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