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Kynurenine 3-Monooxygenase Inhibition in Blood Ameliorates Neurodegeneration
TLDR
Chronic oral administration of JM6 inhibits KMO in the blood, increasing kynurenic acid levels and reducing extracellular glutamate in the brain, and it extends life span, prevents synaptic loss, and decreases microglial activation in a mouse model of Huntington's disease. Expand
Passive Immunization Reduces Behavioral and Neuropathological Deficits in an Alpha-Synuclein Transgenic Model of Lewy Body Disease
TLDR
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. Expand
Patterns of gene dysregulation in the frontal cortex of patients with HIV encephalitis
TLDR
HIV proteins released from infected macrophages might not only induce a neuroinflammatory response, but also may promote neurodegeneration by interfering with neuronal transcription of genes involved in regulating signaling and cytoskeletal molecules important in maintaining synapto-dendritic functioning and integrity. Expand
Neuroprotective Effects of Regulators of the Glycogen Synthase Kinase-3β Signaling Pathway in a Transgenic Model of Alzheimer's Disease Are Associated with Reduced Amyloid Precursor Protein
TLDR
Modulation of the GSK3β signaling pathway might also have neuroprotective effects in tg mice by regulating APP maturation and processing and further supports the notion that G SK3β might be a suitable target for the treatment of AD. Expand
Beclin 1 Gene Transfer Activates Autophagy and Ameliorates the Neurodegenerative Pathology in α-Synuclein Models of Parkinson's and Lewy Body Diseases
TLDR
Beclin 1 plays an important role in the intracellular degradation of α-syn either directly or indirectly through the autophagy pathway and may present a novel therapeutic target for LBD/PD. Expand
Selective Molecular Alterations in the Autophagy Pathway in Patients with Lewy Body Disease and in Models of α-Synucleinopathy
TLDR
This study supports the notion that defects in the autophagy pathway and more specifically in mTor and Atg7 are associated with neurodegeneration in DLB cases and α-synuclein transgenic models and supports the possibility that modulators of the autophile pathway might have potential therapeutic effects. Expand
Alpha-synuclein sequesters Dnmt1 from the nucleus: a novel mechanism for epigenetic alterations in Lewy body diseases.
TLDR
Evidence of reduction of nuclear Dnmt1 levels in human postmortem brain samples from PD and DLB patients as well as in the brains of α-synuclein transgenic mice models is presented, indicating a novel mechanism for epigenetic dysregulation in Lewy body diseases. Expand
Increased BMP6 Levels in the Brains of Alzheimer's Disease Patients and APP Transgenic Mice Are Accompanied by Impaired Neurogenesis
TLDR
It is suggested that Aβ-associated increases in BMP6 expression in AD may have deleterious effects on neurogenesis in the hippocampus, and therapeutic approaches could focus on normalization of B MP6 levels to protect against AD-related neurogenic deficits. Expand
Neurodegeneration in a Transgenic Mouse Model of Multiple System Atrophy Is Associated with Altered Expression of Oligodendroglial-Derived Neurotrophic Factors
TLDR
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. Expand
Aβ vaccination effects on plaque pathology in the absence of encephalitis in Alzheimer disease
TLDR
A patient with Alzheimer disease (AD) without encephalitis who was immunized with AN-1792 (an adjuvanted formulation of Aβ-42) illustrates the effects of an A β-based immunization on AD pathogenesis in the absence of overt meningoencephalitis and leukoencephalopathy. Expand
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