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Factors responsible for neurofibrillary tangles and neuronal cell losses in tauopathy
Author(s) -
Wakasaya Yasuhito,
Kawarabayashi Takeshi,
Watanabe Mitsunori,
YamamotoWatanabe Yukiko,
Takamura Ayumi,
Kurata Tomoko,
Murakami Tetsuro,
Abe Koji,
Yamada Kiyofumi,
Wakabayashi Koichi,
Sasaki Atsushi,
Westaway David,
Hyslop Peter St. George,
Matsubara Etsuro,
Shoji Mikio
Publication year - 2011
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22572
Subject(s) - tauopathy , biology , neurofibrillary tangle , transactivation , neurodegeneration , microbiology and biotechnology , neuroscience , biochemistry , gene , gene expression , alzheimer's disease , senile plaques , pathology , medicine , disease
TgTauP301L mice that overexpress the mutant human tauP301L present in FTDP‐17 reproduce neurofibrillary tangles (NFTs), neuronal cell losses, memory disturbance, and substantial phenotypic variation. To demonstrate factors responsible for NFT formation and neuronal cell losses, sets of TgTauP301L for comparison with or without NFTs and neuronal cell losses were studied with oligonucleotide microarrays. Gene expressions were altered in biological pathways, including oxidative stress, apoptosis, mitochondrial fatty acid betaoxidation, inflammatory response pathway, and complement and coagulation cascade pathways. Among 24 altered genes, increased levels of apolipoprotein D (ApoD) and neuronal PAS domain protein 4 (Npas4) and decreased levels of doublecortin (DCX) and potassium channel, voltage‐gated, shaker‐related subfamily, β member 1 (Kcnab1) were found in the TgTauP301L with NFTs and neuronal cell losses, Alzheimer's brains, and tauopathy brains. Thus, many biological pathways and novel molecules are associated with NFT formation and neuronal cell losses in tauopathy brains. © 2011 Wiley‐Liss, Inc.