Scholars@Duke publication: Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology.

Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology.

Publication , Journal Article

Wang, C; Wilson, WA; Moore, SD; Mace, BE; Maeda, N; Schmechel, DE; Sullivan, PM

Published in: Neurobiol Dis

March 2005

The human APOE*4 allele is associated with an early age of onset and increased risk of Alzheimer's disease (AD). Long before the onset of AD, cognitive deficits can be identified in APOE*4 carriers. We examined neurons in the lateral amygdala of young apolipoprotein (apo) E3 and apoE4 targeted replacement (TR) mice for changes in synaptic integrity. ApoE4 mice displayed significantly reduced excitatory synaptic transmission and dendritic arborization. Despite these changes there were no signs of gliosis, amyloid deposition or neurofibrillary tangles in these mice. To our knowledge, this is the first study to suggest that cognitive deficits in APOE*4 carriers are due to inherent defects in synaptic function that appear prior to any age-dependent markers of neuropathology.

Duke Scholars

Author Scott Daniel Moore Psychiatry & Behavioral Sciences, Adult Psychiatry & Psychol ...

Author Patrick Sullivan Medicine, Geriatrics

Published In

Neurobiol Dis

DOI

10.1016/j.nbd.2004.10.013

ISSN

0969-9961

Publication Date

March 2005

Volume

Issue

Start / End Page

390 / 398

Location

United States

Related Subject Headings

Synaptic Transmission
Synapses
Neurology & Neurosurgery
Mice, Transgenic
Mice
Memory Disorders
Male
Humans
Gene Targeting
Excitatory Postsynaptic Potentials

Citation

APA

Chicago

ICMJE

MLA

NLM

Wang, C., Wilson, W. A., Moore, S. D., Mace, B. E., Maeda, N., Schmechel, D. E., & Sullivan, P. M. (2005). Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology. Neurobiol Dis, 18(2), 390–398. https://doi.org/10.1016/j.nbd.2004.10.013

Wang, Chunsheng, Wilkie A. Wilson, Scott D. Moore, Brian E. Mace, Nobuyo Maeda, Donald E. Schmechel, and Patrick M. Sullivan. “Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology.” Neurobiol Dis 18, no. 2 (March 2005): 390–98. https://doi.org/10.1016/j.nbd.2004.10.013.

Wang C, Wilson WA, Moore SD, Mace BE, Maeda N, Schmechel DE, et al. Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology. Neurobiol Dis. 2005 Mar;18(2):390–8.

Wang, Chunsheng, et al. “Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology.” Neurobiol Dis, vol. 18, no. 2, Mar. 2005, pp. 390–98. Pubmed, doi:10.1016/j.nbd.2004.10.013.

Wang C, Wilson WA, Moore SD, Mace BE, Maeda N, Schmechel DE, Sullivan PM. Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology. Neurobiol Dis. 2005 Mar;18(2):390–398.

Published In

Neurobiol Dis

DOI

10.1016/j.nbd.2004.10.013

ISSN

0969-9961

Publication Date

March 2005

Volume

Issue

Start / End Page

390 / 398

Location

United States

Related Subject Headings

Synaptic Transmission
Synapses
Neurology & Neurosurgery
Mice, Transgenic
Mice
Memory Disorders
Male
Humans
Gene Targeting
Excitatory Postsynaptic Potentials