Demonstrated that reducing brain levels of the protein tau prevents Alzheimer-related memory deficits in mouse models of the disease
Discovered that amyloid proteins may contribute to cognitive deficits in Alzheimer’s disease by causing seizure-like activity in memory centers of the brain
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Identified a novel way to prevent the disease-causing buildup of amyloid proteins through a naturally occurring amyloid degrading enzyme
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Discovered that blocking an inflammatory signaling pathway in the brain’s immune cells, microglia, can diminish the neurotoxicity of amyloid proteins
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Demonstrated that the major genetic risk factor for Alzheimer’s disease, apolipoprotein E4, is cleaved into toxic fragments that impair mitochondrial energy production in neurons
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Identified apolipoprotein E4-related drug targets that are now being used for the development of novel Alzheimer treatments
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Identified components of a molecular complex that is critical for the development of neuronal branches (dendrites) and has been implicated in frontotemporal dementia
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Discovered that aggregation of the protein causing Huntington’s disease actually serves a protective function
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Identified novel therapeutic targets for the treatment of Huntington’s disease and Parkinson’s disease using yeast genetics
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Identified the endogenous cannabinoid signaling system as a novel therapeutic target for treating Parkinson’s disease
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Discovered that a blood protein, fibrinogen, may elicit inflammatory neurological conditions such as multiple sclerosis and developed treatments to block its disease-causing effects
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Discovered that a neurotrophin receptor, p75NTR, can regulate fibrosis and tissue repair
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Revealed the unique role of a small non-coding RNA, microRNA-9a, in the development of the nervous system
To see more scientific achievements and further information about research at the Gladstone Institute of Neurological Disease, please see the Investigator and News pages.
