Alexander Gerhard

TL;DR: The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases, and a large hexanucleotide repeat expansion in the first intron of C9ORF72 is shown.

TL;DR: In vivo findings confirm that widespread microglial activation is associated with the pathological process in PD and suggest that microglia are activated early in the disease process, and levels then remain relatively static, possibly driving the disease via cytokine release.

TL;DR: Mutations in the C9ORF72 gene may be a major cause not only of frontotemporal dementia with motor neuron disease but also of late onset psychosis, and the behavioural characteristics of patients with C9 ORF72 mutations are qualitatively distinct.

TL;DR: The inverse correlation between MMSE and microglial activation is compatible with a role of microglia in neuronal damage and the localisation of these increases to association areas is confirmed.

TL;DR: Findings show that the level of microglial activation correlates with Huntington disease (HD) severity, and lend support to the view that microglia contribute to the ongoing neuronal degeneration in HD and indicate that [11C](R)-PK11195 PET provides a valuable marker when monitoring the efficacy of putative neuroprotecting agents in this relentlessly progressive genetic disorder.