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P1–053: Alzheimer's disease neuropathology is not mitigated by the physiological expression of human ABCA1 in APP/PS1 mice
Author(s) -
Hirsch-Reinshagen Veronica,
Chan Jeniffer Y.,
McIsaac Sean A.,
Naus Kathryn E.,
Maia Luis F.,
Burgess Braydon L.,
Singaraja Roshni R.,
Hayden Michael R.,
Wellington Cheryl L.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.428
Subject(s) - abca1 , apolipoprotein e , neuropathology , genetically modified mouse , transgene , endocrinology , medicine , amyloid (mycology) , neurodegeneration , biology , alzheimer's disease , amyloid precursor protein , cholesterol , transporter , disease , biochemistry , gene , botany
a reduction in synapse density per se is unlikely to underlie the cognitive deficits present in TASTPM mice from 6 months of age and the presence of -amyloid plaques may not be sufficient to cause synaptic die-back. However, the current morphological analysis could not elucidate the functional status of synapses. Moreover, at 6 10 months of age synaptic sprouting contemporaneous with a degenerative process may be sufficient to maintain synaptic density but not synaptic function and synapse loss in TASTPM mice may eventually be manifest at greater ages.