Targeting Aß oligomers [electronic resource] : a molecular basis for the cause, diagnosis, and treatment of Alzheimer's disease / William L. Klein.

By: Klein, William L [spk]Material type: FilmFilmSeries: Henry Stewart talksBiomedical & life sciences collection. Drug discovery and development in the neurosciences: Publisher: London : Henry Stewart Talks, 2014Description: 1 online resource (1 streaming video file (68 min.) : color, sound)Other title: Amyloid beta oligomers : pathogenic ligands that attack dendritic spines | Aß oligomers : pathogenic ligands that attack dendritic spines | Targeting AB oligomers | Targeting amyloid beta oligomersSubject(s): Alzheimer's disease -- Chemotherapy | Alzheimer's disease -- Diagnosis | Alzheimer's disease -- Pathogenesis | Amyloid beta-protein | Nervous system -- Degeneration | Alzheimer Disease -- drug therapy | Alzheimer Disease -- etiology | Alzheimer Disease -- metabolism | Alzheimer Disease -- pathology | Amyloid beta-Peptides -- metabolism | Brain -- metabolism | Neurodegenerative Diseases -- metabolism | Neurons -- metabolism | Neurons -- pathologyOnline resources: Click here to access online | Series
Contents:
Contents: The oligomer cascade hypothesis for Alzheimer's Disease -- Why the oligomer hypothesis has largely supplanted the amyloid cascade hypothesis -- The role of AβOs in memory failure and the major facets of AD neuropathology -- Mechanisms by which AβOs instigate neurotoxicity -- Why AβOs accumulate in the first place -- How AβOs offer superb targets for novel AD diagnostics and disease-modifying therapeutics -- Beside its direct link to Alzheimer's disease, the discovery of toxic Aβ oligomers has provided a novel structural archetype for toxins germane to more than two dozen diseases of protein mis-folding, including Diabetes, Parkinson's, and prion diseases.
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Animated audio-visual presentation with synchronized narration.

Title from title frames.

Contents: The oligomer cascade hypothesis for Alzheimer's Disease -- Why the oligomer hypothesis has largely supplanted the amyloid cascade hypothesis -- The role of AβOs in memory failure and the major facets of AD neuropathology -- Mechanisms by which AβOs instigate neurotoxicity -- Why AβOs accumulate in the first place -- How AβOs offer superb targets for novel AD diagnostics and disease-modifying therapeutics -- Beside its direct link to Alzheimer's disease, the discovery of toxic Aβ oligomers has provided a novel structural archetype for toxins germane to more than two dozen diseases of protein mis-folding, including Diabetes, Parkinson's, and prion diseases.

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