Several years ago, Karen Hsiao and colleagues at the University of Minnesota reported that mice containing an FAD mutant form of the human amyloid precursor protein (APP) are impaired in their ability to learn. These mice, however, do not exhibit structural damage or neuronal loss. This observation fueled speculation that the FAD mutation might be exerting more subtle damage to neuronal function. Now Hsiao’s team think they have detected just such a change. In the March issue of Nature Neuroscience, they report that these transgenic mice are deficient in long-term potentiation, or LTP, a process widely thought to provide the neural basis of learning and memory. In the Hsiao mice, the LTP deficits worsen with age, and also tended to be correlated with poorer memory. The authors suggest that the APP mutation may contribute to Alzheimer’s by impairing the ability of neurons to modify synapses.-June Kinoshita.
References: Chapman PF, White GL, Jones MW, Cooper-Blacketer D, Marshall VJ, Irizarry M, Younkin L, Good MA, Bliss TV, Hyman BT, Younkin SG, Hsiao KK. Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nat Neurosci 1999 Mar;2(3):271-6. Abstract

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  1. . Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nat Neurosci. 1999 Mar;2(3):271-6. PubMed.

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  1. . Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nat Neurosci. 1999 Mar;2(3):271-6. PubMed.