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      Synaptic Impairment in Alzheimer's Disease: A Dysregulated Symphony.

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          Abstract

          Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodegeneration, not only as a result of the extracellular accumulation of beta-amyloid peptide (Aβ) and intracellular accumulation of tau, but also as a consequence of the dysfunction and loss of synapses. Although significant advances have been made in our understanding of the relationship of the pathological role of Aβ and tau in synapse dysfunction, several questions remain as to how Aβ and tau interdependently cause impairments in synaptic function in AD. Overall, more insight into these questions should enable researchers in this field to develop novel therapeutic targets to mitigate or delay the cognitive deficits associated with this devastating disease.

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          Author and article information

          Journal
          Trends Neurosci.
          Trends in neurosciences
          Elsevier BV
          1878-108X
          0166-2236
          May 08 2017
          Affiliations
          [1 ] Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA.
          [2 ] Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA; Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA. Electronic address: laferla@uci.edu.
          Article
          S0166-2236(17)30069-3
          10.1016/j.tins.2017.04.002
          28494972
          7170fb48-7285-470c-a50b-ad0fbfea3ee8
          History

          Alzheimer’s disease,beta-amyloid,synaptic impairment,tau

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