Alix de Calignon

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Neurofibrillary tangles advance from layer II of the entorhinal cortex (EC-II) toward limbic and association cortices as Alzheimer's disease evolves. However, the mechanism involved in this hierarchical pattern of disease progression is unknown. We describe a transgenic mouse model in which overexpression of human tau P301L is restricted to EC-II. Tau(More)
Pol32 is a subunit of Saccharomyces cerevisiae DNA polymerase δ required in DNA replication and repair. To gain insight into the function of Pol32 and to determine in which repair pathway POL32 may be involved, we extended the analysis of the pol32Δ mutant with respect to UV and methylation sensitivity, UV-induced mutagenesis; and we performed an epistasis(More)
Tara L. Spires-Jones,1 Alix de Calignon,1 Toshifumi Matsui,1 Cindy Zehr,3 Rose Pitstick,4 Hai-Yan Wu,1 Jennifer D. Osetek,1 Phillip B. Jones,1,2 Brian J. Bacskai,1 Mel B. Feany,5 George A. Carlson,4 Karen H. Ashe,6 Jada Lewis,3 Bradley T. Hyman1 1MassGeneral Institute for Neurodegenerative Disease and 2Martinos Center for Biomedical Imaging, Massachusetts(More)
Senile plaques accumulate over the course of decades in the brains of patients with Alzheimer’s disease. A fundamental tenet of the amyloid hypothesis of Alzheimer’s disease is that the deposition of amyloid-b precedes and induces the neuronal abnormalities that underlie dementia. This idea has been challenged, however, by the suggestion that alterations in(More)
Neurofibrillary tangles are intracellular accumulations of hyperphosphorylated and misfolded tau protein characteristic of Alzheimer’s disease and other tauopathies. Classic cross-sectional studies of Alzheimer patient brains showed associations of tangle accumulation with neuronal loss, synapse loss, and dementia, which led to the supposition that tangles(More)
Background: Immunization against amyloid-b (Ab), the peptide that accumulates in the form of senile plaques and in the cerebrovasculature in Alzheimer’s disease (AD), causes a dramatic immune response that prevents plaque formation and clears accumulated Ab in transgenic mice. In a clinical trial of Ab immunization, some patients developed(More)
Manuela Polydoro,1 Alix de Calignon,1 Marc Suárez-Calvet,1,2 Laura Sanchez,1 Kevin R. Kay,1 Samantha B. Nicholls,1 Allyson D. Roe,1 Rose Pitstick,3 George A. Carlson,3 Teresa Gómez-Isla,1,2 Tara L. Spires-Jones,1 and Bradley T. Hyman1 1MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Alzheimer’s Disease Research Laboratory,(More)
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