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ARTICLESir, We thank Dr Vishnu for his interest in our paper. We reported atrophy of the caudate and thalamus in presymptomatic familial Alzheimer’s disease mutation carriers at a stage when hippocampal atrophy was not yet evident (Ryan et al. , 2013). As Dr Vishnu (2013) describes, brain atrophy on MRI is thought to be a biomarker of neuronal loss, which is considered to be a downstream element in the amyloid cascade hypothesis of Alzheimer’s disease pathogenesis. Dr Vishnu raises the question of whether the caudate and thalamic atrophy we detected represents neuronal injury induced by amyloid or by amyloid-independent mechanisms. We agree that this is an important point and feel that it in fact highlights an even broader issue; that it is not yet clear what pathological processes do account for the volume or other MRI-based changes that may be witnessed in the presymptomatic phase of Alzheimer’s disease. Although there are numerous clinicopathological studies correlating atrophy on MRI with neuronal loss, Braak neurofibrillary tangle stage and tau burden in patients with established symptomatic Alzheimer’s disease (Zarow et al. , 2005; Whitwell et al. , 2008), this information is lacking for the presymptomatic stage. Various different processes may give rise to changes in the volume of brain structures, some of which may be dynamic, and this uncertainty should be taken into account in hypothetical biomarker models of presymptomatic Alzheimer’s disease.We proposed in our article (Ryan et al. , 2013) that axonal injury and subsequent degeneration may account for the thalamic and …

Reply: Implications of presymptomatic change in thalamus and caudate in Alzheimer’s disease