The bad seed in Alzheimer's disease

John D. Fryer; David M. Holtzman

doi:10.1016/j.neuron.2005.07.002

The bad seed in Alzheimer's disease

John D. Fryer, David M. Holtzman

Neuroscience

Research output: Contribution to journal › Short survey › peer-review

15 Scopus citations

Abstract

In this issue of Neuron, McGowan et al. report on a new mouse model of amyloid deposition as occurs in Alzheimer's disease. Unlike previous models in which overexpression of the amyloid precursor protein results in amyloid plaque formation, McGowan et al. have produced mice that overexpress only Aβ40 or Aβ42 and prove that Aβ42 is critical for the formation of amyloid deposits in vivo.

Original language	English (US)
Pages (from-to)	167-168
Number of pages	2
Journal	Neuron
Volume	47
Issue number	2
DOIs	https://doi.org/10.1016/j.neuron.2005.07.002
State	Published - Jul 21 2005

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neuron.2005.07.002

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title = "The bad seed in Alzheimer's disease",

abstract = "In this issue of Neuron, McGowan et al. report on a new mouse model of amyloid deposition as occurs in Alzheimer's disease. Unlike previous models in which overexpression of the amyloid precursor protein results in amyloid plaque formation, McGowan et al. have produced mice that overexpress only Aβ40 or Aβ42 and prove that Aβ42 is critical for the formation of amyloid deposits in vivo.",

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AB - In this issue of Neuron, McGowan et al. report on a new mouse model of amyloid deposition as occurs in Alzheimer's disease. Unlike previous models in which overexpression of the amyloid precursor protein results in amyloid plaque formation, McGowan et al. have produced mice that overexpress only Aβ40 or Aβ42 and prove that Aβ42 is critical for the formation of amyloid deposits in vivo.

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The bad seed in Alzheimer's disease

Abstract

ASJC Scopus subject areas

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