In search of the soluble

Article Abstract:

The pathogenesis of Alzheimer's disease results from mutations affecting the beta-amyloid precursor protein (APP). Three research groups have ascertained that amyloid metabolism is the prime factor in generating the familial, early onset form of this disease. The research groups consisted of Christian Haass and colleagues, Peter Seubert and colleagues, S.G. Younkin and colleagues and the as yet unpublished work of B. Yankner. The next step is to find out how APP metabolism can be controlled to prevent or treat Alzheimer's disease.

Health aspects, Development and progression, Mutation (Biology), Mutation

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Mouse model made

Article Abstract:

Transgenic mice having mutation in the beta-amyloid precursor protein (APP) gene serve as models for studying the development of Alzheimer's disease (AD). An APP Val to Phe mutation in residue 717 induces symptoms similar to those of AD. These mice exhibit severe cortical and hippocampal pathology despite the absence of neurofibrillary tangles. These observations will be useful in studies on AD therapy and neurochemistry.

Models, Genetically modified mice, Neurochemistry

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Abeta peptide vaccination prevents memory loss n an animal model of Alzheimer's disease

Article Abstract:

Abeta peptide vaccination is found to prevent memory loss in an animal model of Alzheimer's disease.

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