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      Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease.

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          Abstract

          Neural network dysfunction may play an important role in Alzheimer's disease (AD). Neuronal circuits vulnerable to AD are also affected in human amyloid precursor protein (hAPP) transgenic mice. hAPP mice with high levels of amyloid-beta peptides in the brain develop AD-like abnormalities, including cognitive deficits and depletions of calcium-related proteins in the dentate gyrus, a region critically involved in learning and memory. Here, we report that hAPP mice have spontaneous nonconvulsive seizure activity in cortical and hippocampal networks, which is associated with GABAergic sprouting, enhanced synaptic inhibition, and synaptic plasticity deficits in the dentate gyrus. Many Abeta-induced neuronal alterations could be simulated in nontransgenic mice by excitotoxin challenge and prevented in hAPP mice by blocking overexcitation. Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD.

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          Author and article information

          Journal
          Neuron
          Neuron
          Elsevier BV
          0896-6273
          0896-6273
          Sep 06 2007
          : 55
          : 5
          Affiliations
          [1 ] Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA. jpalop@gladstone.ucsf.edu
          Article
          S0896-6273(07)00570-3 NIHMS1553440
          10.1016/j.neuron.2007.07.025
          8055171
          17785178
          456a8d97-c238-4d3b-9d64-b58afafd6aed
          History

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