APP variants such as the London mutant generate larger amounts of amyloid-β peptide (1–42)92 and soluble oAβ has been proposed to contribute to loss of synapses at an early stage of neurodegeneration in Alzheimer’s disease.93 We analysed the consequences of oAβ on the behaviour of spine-invading microtubules in cultured hippocampal neurons. The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.