Frank M. LaFerla
University of California, Irvine
291 Papers
1.5K Citations
Frank M. LaFerla is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Alzheimer's disease & Biology. The author has an hindex of 103, co-authored 274 publications. Previous affiliations of Frank M. LaFerla include University of California, Berkeley & University of California.
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Papers
Calcium dysregulation in Alzheimer's disease: recent advances gained from genetically modified animals.
TL;DR: Recent contributions that transgenic technology has brought to the field of neurodegeneration are discussed and it is likely that amyloid-beta and its ability to disrupt intracellular calcium homeostasis plays a key role in this process.
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The role of nicotinic acetylcholine receptors in Alzheimer's disease.
Salvatore Oddo,Frank M. LaFerla +1 more
TL;DR: The role of nicotinic acetylcholine receptors in transgenic models and in AD is considered, as they offer a means to gain mechanistic insights into the disease process in an in vivo setting.
136
Chronic copper exposure exacerbates both amyloid and tau pathology and selectively dysregulates cdk5 in a mouse model of AD.
TL;DR: Chronic copper exposure accelerates not only amyloid pathology but also tau pathology in a mouse model of AD, and changes were found to be mediated via up‐regulation of BACE1 as significant increases in Bace1 levels and deposits were detected around plaques in mice following copper exposure.
135
Oligemic Hypoperfusion Differentially Affects Tau and Amyloid-β
TL;DR: This study indicates for the first time that total tau and amyloid-beta are differentially impacted by mild hypoperfusion, and results in a significant increase specifically in tau phosphorylated at serine and threonine and a tau epitope associated with paired helical filaments in AD patients.
135
Inclusion body myositis-like phenotype induced by transgenic overexpression of βAPP in skeletal muscle
Michael C. Sugarman,Tritia R. Yamasaki,Salvatore Oddo,Julio C. Echegoyen,M. Paul Murphy,Todd E. Golde,Mehrdad Jannatipour,Malcolm A. Leissring,Frank M. LaFerla +8 more
TL;DR: Transgenic mice were derived in which selective overexpression of βAPP leads to the development of a subset of other histopathological and clinical features characteristic of IBM, including centric nuclei, inflammation, and deficiencies in motor performance, consistent with a pathogenic role for βAPP mismetabolism in human IBM.
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