| Literature DB >> 22512241 |
Keith A Vossel1, Nga Bien-Ly, Aubrey Bernardo, Katya Rascovsky, Anna Karydas, Gil D Rabinovici, Manu Sidhu, Eric J Huang, Bruce L Miller, Yadong Huang, William W Seeley.
Abstract
Frontotemporal lobar degeneration with motor neuron disease (FTLD-MND) is characterized by neuronal cytoplasmic inclusions containing TDP-43. Apolipoprotein E4 (apoE4), derived from the apoE ϵ4 allele, enhances brain atrophy in FTLD through unknown mechanisms. Here, we studied two siblings with C9ORF72-linked familial FTLD-MND, an apoE ϵ4 homozygote and an apoE ϵ3 homozygote. The apoE ϵ4 homozygote had more cognitive-behavioral symptoms, fronto-insulo-temporal atrophy, and apoE fragments and aggregates in the anterior cingulate cortex. ApoE formed complexes with TDP-43 that were more abundant in the apoE ϵ4 homozygote. Although differences seen in a sibling pair could arise due to chance, these findings raise the possibility that apoE4 exacerbates brain pathology in FTLD through formation of neurotoxic apoE fragments and interactions with TDP-43.Entities:
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Year: 2012 PMID: 22512241 PMCID: PMC3655113 DOI: 10.1080/13554794.2012.667124
Source DB: PubMed Journal: Neurocase ISSN: 1355-4794 Impact factor: 0.881