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What Happens with the Circuit in Alzheimer's Disease in Mice and Humans?

Zott, Benedikt, Busche, Marc Aurel, Sperling, Reisa A., Konnerth, Arthur·2018·Annual Review of Neuroscience
DOI 10.1146/annurev-neuro-080317-061725PMC PMC6571139
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Abstract

A major mystery of many types of neurological and psychiatric disorders, such as Alzheimer's disease (AD), remains the underlying, disease-specific neuronal damage. Because of the strong interconnectivity of neurons in the brain, neuronal dysfunction necessarily disrupts neuronal circuits. In this article, we review evidence for the disruption of large-scale networks from imaging studies of humans and relate it to studies of cellular dysfunction in mouse models of AD. The emerging picture is that some forms of early network dysfunctions can be explained by excessively increased levels of neuronal activity. The notion of such neuronal hyperactivity receives strong support from in vivo and in vitro cellular imaging and electrophysiological recordings in the mouse, which provide mechanistic insights underlying the change in neuronal excitability. Overall, some key aspects of AD-related neuronal dysfunctions in humans and mice are strikingly similar and support the continuation of such a translational strategy.

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Metadata

Authors
Zott, B., Busche, M. A., Sperling, R. A., & Konnerth, A.
Affiliations
  • Institute of Neuroscience, Technical University of Munich, 80802 Munich, Germany;
  • MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
  • Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
Venue
Annual Review of Neuroscience
Publisher
Annual Reviews
Published
2018-07-08
Volume
41
Issue
1
Pages
277-297
ISSN
  • 0147-006X
  • 1545-4126
DOI
10.1146/annurev-neuro-080317-061725
PMC
PMC6571139
Cited by
221
References
49
Language
en

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