Deposition of Aβ-amyloid occurs in parenchymal plaques and also as vascular deposits in amyloid angiopathy. Allen et al. have now sought to define phenotypic heterogeneity in amyloid deposition in Alzheimer’s disease and its relationship to clinical and genetic factors. They have found that amyloid deposition can be classified into four patterns, depending on relative deposition in plaques and vessels. CAA with capillary involvement (type 3) is particularly associated with possession of the APOE ε4 allele, KU-60019 suggesting an influence of genetics on pattern of deposition. This new classification scheme refines our knowledge of the distribution of

Aβ-pathology in Alzheimer’s disease and will be a useful tool for studies of phenotypic subtypes of Alzheimer’s disease. Progressive supranuclear palsy (PSP) is a tauopathy that may present as several different clinical variants. Ling et al. have now compared the pathology of cases of PSP presenting with the corticobasal selleck chemicals syndrome (PSP-CBS) to that of cases presenting with the classical Richardson’s syndrome (PSP-RS). Protein analysis confirms 4R tau deposition

in both groups and there is no difference in tau haplotype between these groups. Morphometric studies of tau pathology shows a shift of tau pathology load from basal ganglia to cortical regions in PSP-CBS compared to PSP-RS, suggesting that PSP-CBS is a cortical variant of CBS. Fasciculation and elongation protein zeta 1 (FEZ1) has been implicated in embryonic development of the

central nervous system and has a role in neurite outgrowth. There is also evidence that it has a role in regulating the dopaminergic neuron differentiation Cytidine deaminase and dopamine release, raising the question of whether it has a role in the pathogenesis of Parkinson’s disease. Sun et al. have investigated FEZ1 in a model system in which dopaminergic deficit and neuron loss is induced using 6-hydroxydopamine hydrobromide. They show that FEZ1 is expressed in adult striatum and substantia nigra. Expression increases in the model, but also shows a shift in localisation, with decreasing FEZ1 in tyrosine hydroxylase positive dopaminergic neurons and an increase in reactive astrocytes. Astrocytes have been suggested to have a protective role for dopaminergic neurons during Parkinson’s disease progression, and these results suggest that FEZ1 may have a role in this response. Hippocampal sclerosis, characterised by neuronal loss and gliosis, is seen in association with epilepsy, particularly in relation to mesial temporal sclerosis. However, hippocampal sclerosis also occurs in the elderly in association with memory impairment and dementia, where is may be associated with neurodegenerative pathologies such as Alzheimer’s disease and TDP-43 pathology.