Synapses, synaptic activity and intraneuronal Aβ in Alzheimer's disease
Tampellini, Davide LU and Gouras, Gunnar K. LU
(2010)
In Frontiers in Aging Neuroscience
2(MAY).
- Abstract
β-Amyloid peptide accumulation plays a central role in the pathogenesis of Alzheimer's disease. Aberrant β-amyloid buildup in the brain has been shown to be present both in the extracellular space and within neurons. Synapses are important targets of β-amyloid, and alterations in synapses better correlate with cognitive impairment than amyloid plaques or neurofibrillary tangles. The link between β-amyloid and synapses became even tighter when it was discovered that β-amyloid accumulates within synapses and that synaptic activity modulates β-amyloid secretion. Currently, a central question in Alzheimer's disease research is what role synaptic activity plays in the disease process, and how specifically β-amyloid is involved in the... (More)
β-Amyloid peptide accumulation plays a central role in the pathogenesis of Alzheimer's disease. Aberrant β-amyloid buildup in the brain has been shown to be present both in the extracellular space and within neurons. Synapses are important targets of β-amyloid, and alterations in synapses better correlate with cognitive impairment than amyloid plaques or neurofibrillary tangles. The link between β-amyloid and synapses became even tighter when it was discovered that β-amyloid accumulates within synapses and that synaptic activity modulates β-amyloid secretion. Currently, a central question in Alzheimer's disease research is what role synaptic activity plays in the disease process, and how specifically β-amyloid is involved in the synaptic dysfunction that characterizes the disease.
(Less)
- author
- Tampellini, Davide
LU
and Gouras, Gunnar K.
LU
- publishing date
- 2010-05-21
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alzheimer disease, Amyloid, Amyloid precursor protein, Neprilysin, Neurodegeneration, Neuron, Synapse, Synaptic plasticity
- in
- Frontiers in Aging Neuroscience
- volume
- 2
- issue
- MAY
- article number
- 13
- publisher
- Frontiers Media S. A.
- external identifiers
-
- scopus:84885915876
- ISSN
- 1663-4365
- DOI
- 10.3389/fnagi.2010.00013
- language
- English
- LU publication?
- no
- id
- 54a2cdd9-2209-4abf-95ee-0130a57acd41
- date added to LUP
- 2020-02-20 14:15:26
- date last changed
- 2022-02-01 03:46:11
@article{54a2cdd9-2209-4abf-95ee-0130a57acd41,
abstract = {{<p>β-Amyloid peptide accumulation plays a central role in the pathogenesis of Alzheimer's disease. Aberrant β-amyloid buildup in the brain has been shown to be present both in the extracellular space and within neurons. Synapses are important targets of β-amyloid, and alterations in synapses better correlate with cognitive impairment than amyloid plaques or neurofibrillary tangles. The link between β-amyloid and synapses became even tighter when it was discovered that β-amyloid accumulates within synapses and that synaptic activity modulates β-amyloid secretion. Currently, a central question in Alzheimer's disease research is what role synaptic activity plays in the disease process, and how specifically β-amyloid is involved in the synaptic dysfunction that characterizes the disease.</p>}},
author = {{Tampellini, Davide and Gouras, Gunnar K.}},
issn = {{1663-4365}},
keywords = {{Alzheimer disease; Amyloid; Amyloid precursor protein; Neprilysin; Neurodegeneration; Neuron; Synapse; Synaptic plasticity}},
language = {{eng}},
month = {{05}},
number = {{MAY}},
publisher = {{Frontiers Media S. A.}},
series = {{Frontiers in Aging Neuroscience}},
title = {{Synapses, synaptic activity and intraneuronal Aβ in Alzheimer's disease}},
url = {{http://dx.doi.org/10.3389/fnagi.2010.00013}},
doi = {{10.3389/fnagi.2010.00013}},
volume = {{2}},
year = {{2010}},
}