Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses
Takahashi, Reisuke H. ; Capetillo-Zarate, Estibaliz ; Lin, Michael T. ; Milner, Teresa A. and Gouras, Gunnar K. LU
(2010)
In Neurobiology of Aging
31(7).
p.1145-1152
- Abstract
Although β-amyloid (Aβ) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Aβ and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precursor protein (APP) Swedish mutant transgenic mice, and since neurofibrillary tangles develop in triple transgenic mice harboring mutations in APP, tau and presenilin 1, we utilized these well-characterized mouse models to explore the relation between Aβ and tau pathologies. We now report that pathological accumulation of Aβ and... (More)
Although β-amyloid (Aβ) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Aβ and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precursor protein (APP) Swedish mutant transgenic mice, and since neurofibrillary tangles develop in triple transgenic mice harboring mutations in APP, tau and presenilin 1, we utilized these well-characterized mouse models to explore the relation between Aβ and tau pathologies. We now report that pathological accumulation of Aβ and hyperphosphorylation of tau develop concomitantly within synaptic terminals.
(Less)
- author
- Takahashi, Reisuke H.
; Capetillo-Zarate, Estibaliz
; Lin, Michael T.
; Milner, Teresa A.
and Gouras, Gunnar K.
LU
- publishing date
- 2010-07
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alzheimer's disease, Amyloid, Electron microscopy, Endosomes, Hippocampus, Microtubules, Neuropathology, Synapse, Tau
- in
- Neurobiology of Aging
- volume
- 31
- issue
- 7
- pages
- 1145 - 1152
- publisher
- Elsevier
- external identifiers
-
- pmid:18771816
- scopus:77952878634
- ISSN
- 0197-4580
- DOI
- 10.1016/j.neurobiolaging.2008.07.021
- language
- English
- LU publication?
- no
- id
- 03073a5d-43e8-4eb0-b0ed-eb7ceb6ee4c8
- date added to LUP
- 2020-02-20 14:19:53
- date last changed
- 2024-05-29 09:29:03
@article{03073a5d-43e8-4eb0-b0ed-eb7ceb6ee4c8,
abstract = {{<p>Although β-amyloid (Aβ) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Aβ and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precursor protein (APP) Swedish mutant transgenic mice, and since neurofibrillary tangles develop in triple transgenic mice harboring mutations in APP, tau and presenilin 1, we utilized these well-characterized mouse models to explore the relation between Aβ and tau pathologies. We now report that pathological accumulation of Aβ and hyperphosphorylation of tau develop concomitantly within synaptic terminals.</p>}},
author = {{Takahashi, Reisuke H. and Capetillo-Zarate, Estibaliz and Lin, Michael T. and Milner, Teresa A. and Gouras, Gunnar K.}},
issn = {{0197-4580}},
keywords = {{Alzheimer's disease; Amyloid; Electron microscopy; Endosomes; Hippocampus; Microtubules; Neuropathology; Synapse; Tau}},
language = {{eng}},
number = {{7}},
pages = {{1145--1152}},
publisher = {{Elsevier}},
series = {{Neurobiology of Aging}},
title = {{Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses}},
url = {{http://dx.doi.org/10.1016/j.neurobiolaging.2008.07.021}},
doi = {{10.1016/j.neurobiolaging.2008.07.021}},
volume = {{31}},
year = {{2010}},
}