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Fiona Crawford

Researcher at Roskamp Institute

Publications -  218
Citations -  21532

Fiona Crawford is an academic researcher from Roskamp Institute. The author has contributed to research in topics: Apolipoprotein E & Traumatic brain injury. The author has an hindex of 54, co-authored 204 publications receiving 20103 citations. Previous affiliations of Fiona Crawford include University of Antwerp & Archer.

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Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease.

TL;DR: A locus segregating with familial Alzheimer's disease (AD) has been mapped to chromosome 21, close to the amyloid precursor protein (APP) gene as discussed by the authors, which suggests that some cases of AD could be caused by mutations in the APP gene.

Segregation of a missense mutation in the amyloid precursor protein gene with familial alzheimers-disease

TL;DR: It is demonstrated that in this kindred, which shows linkage to chromosome 21 markers, there is a point mutation in the APP gene that causes an amino-acid substitution close to the carboxy terminus of the β-amyloid peptide.
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A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N-terminus of beta-amyloid.

TL;DR: A double mutation at codons 670 and 671 (APP 770 transcript) in exon 16 which co–segregates with the disease in two large (probably related) early–onset Alzheimer's disease families from Sweden is identified.
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Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene

TL;DR: The occurrence of a second allelic variant at codon 717 linked to the Alzheimer's phenotype supports the hypothesis that they are pathogenic mutations.
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Microglial Activation Resulting from CD40-CD40L Interaction After β-Amyloid Stimulation

TL;DR: CD40 expression was increased and abnormal tau phosphorylation was reduced in Tg APPsw animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.