Skip to main content
. Author manuscript; available in PMC: 2015 May 21.
Published in final edited form as: Neuron. 2014 May 21;82(4):756–771. doi: 10.1016/j.neuron.2014.05.004

Figure 5. Pathways involved in normal synaptic plasticity and how they may be affected in AD.

Figure 5

Under normal conditions, LTP promotes recruitment of neurotransmitter receptors to active synapses and causes synapse potentiation, stabilization, and growth. LTD conversely results in synapse depotentiation and spine collapse. Both of these processes are affected in animal models of AD with oligomeric Aβ clearly affecting the calcium and calcineurin pathways involved in these phenomena. Tau overexpression has been observed to affect synaptic function in transgenic models and to be necessary for oligomeric Aβ mediated synapse dysfunction, but the mechanisms by which pathological forms of tau affect synaptic plasticity are less well understood. It is possible that hyperphosphorylation affects microtubule stability and the transport of mitochondria to synapses which could affect synaptic function. The cleavage of tau by caspase 3 has also been observed which could be tied to the non-apoptotic role of caspase 3 in LTD and spine collapse.