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Neuron. 2014 May 21;82(4):756-71. doi: 10.1016/j.neuron.2014.05.004.

The intersection of amyloid beta and tau at synapses in Alzheimer's disease.

Author information

1
Centre for Cognitive and Neural Systems, The University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, UK; The Euan MacDonald Centre, The University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, UK. Electronic address: tara.spires-jones@ed.ac.uk.
2
Massachusetts General Hospital, Harvard Medical School, Neurology, 114 16(th) Street, Charlestown, MA 02129, USA. Electronic address: bhyman@partners.org.

Abstract

The collapse of neural networks important for memory and cognition, including death of neurons and degeneration of synapses, causes the debilitating dementia associated with Alzheimer's disease (AD). We suggest that synaptic changes are central to the disease process. Amyloid beta and tau form fibrillar lesions that are the classical hallmarks of AD. Recent data indicate that both molecules may have normal roles at the synapse, and that the accumulation of soluble toxic forms of the proteins at the synapse may be on the critical path to neurodegeneration. Further, the march of neurofibrillary tangles through brain circuits appears to take advantage of recently described mechanisms of transsynaptic spread of pathological forms of tau. These two key phenomena, synapse loss and the spread of pathology through the brain via synapses, make it critical to understand the physiological and pathological roles of amyloid beta and tau at the synapse.

PMID:
24853936
PMCID:
PMC4135182
DOI:
10.1016/j.neuron.2014.05.004
[Indexed for MEDLINE]
Free PMC Article

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