Increased apolipoprotein E ε4 in epilepsy with senile plaques
Gouras, Gunnar K. LU
; Relkin, Norman R.
; Sweeney, David
; Munoz, David G.
; Mackenzie, Ian R.
and Gandy, Sam
(1997)
In Annals of Neurology
41(3).
p.402-404
- Abstract
Inheritance of the apolipoprotein E (ApoE) ε4 allele is a risk factor for Alzheimer's disease (AD) and is associated with increased deposition of β-amyloid (Aβ) in AD, Down's syndrome, and normal aging. Aβ deposition in the form of senile plaques (SPs) has recently been described in patients with temporal lobe epilepsy (TLE). We studied the relationship between ApoE ε4 genotype and the deposition of Aβ in temporal lobe tissue from patients who underwent temporal lobectomy for intractable epilepsy. TLE patients with SPs had a 70% ApoE ε4 carrier frequency compared with a 27% carrier frequency among age-matched TLE controls without SPs. Our data suggest that the association between ApoE ε4 and intracerebral Aβ accumulation is not unique... (More)
Inheritance of the apolipoprotein E (ApoE) ε4 allele is a risk factor for Alzheimer's disease (AD) and is associated with increased deposition of β-amyloid (Aβ) in AD, Down's syndrome, and normal aging. Aβ deposition in the form of senile plaques (SPs) has recently been described in patients with temporal lobe epilepsy (TLE). We studied the relationship between ApoE ε4 genotype and the deposition of Aβ in temporal lobe tissue from patients who underwent temporal lobectomy for intractable epilepsy. TLE patients with SPs had a 70% ApoE ε4 carrier frequency compared with a 27% carrier frequency among age-matched TLE controls without SPs. Our data suggest that the association between ApoE ε4 and intracerebral Aβ accumulation is not unique to the elderly or to those with dementia, and may be a feature of conditions in which there is both an ApoE ε4 allele and overproduction of Aβ precursor protein, and, presumably, Aβ.
(Less)
- author
- Gouras, Gunnar K.
LU
; Relkin, Norman R.
; Sweeney, David
; Munoz, David G.
; Mackenzie, Ian R.
and Gandy, Sam
- publishing date
- 1997-03
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Annals of Neurology
- volume
- 41
- issue
- 3
- pages
- 402 - 404
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- pmid:9066363
- scopus:0031042358
- ISSN
- 0364-5134
- DOI
- 10.1002/ana.410410317
- language
- English
- LU publication?
- no
- id
- 4a7f66c3-54f9-43f1-9ff0-cc80839adda0
- date added to LUP
- 2020-02-20 14:35:02
- date last changed
- 2024-04-03 03:17:18
@article{4a7f66c3-54f9-43f1-9ff0-cc80839adda0,
abstract = {{<p>Inheritance of the apolipoprotein E (ApoE) ε4 allele is a risk factor for Alzheimer's disease (AD) and is associated with increased deposition of β-amyloid (Aβ) in AD, Down's syndrome, and normal aging. Aβ deposition in the form of senile plaques (SPs) has recently been described in patients with temporal lobe epilepsy (TLE). We studied the relationship between ApoE ε4 genotype and the deposition of Aβ in temporal lobe tissue from patients who underwent temporal lobectomy for intractable epilepsy. TLE patients with SPs had a 70% ApoE ε4 carrier frequency compared with a 27% carrier frequency among age-matched TLE controls without SPs. Our data suggest that the association between ApoE ε4 and intracerebral Aβ accumulation is not unique to the elderly or to those with dementia, and may be a feature of conditions in which there is both an ApoE ε4 allele and overproduction of Aβ precursor protein, and, presumably, Aβ.</p>}},
author = {{Gouras, Gunnar K. and Relkin, Norman R. and Sweeney, David and Munoz, David G. and Mackenzie, Ian R. and Gandy, Sam}},
issn = {{0364-5134}},
language = {{eng}},
number = {{3}},
pages = {{402--404}},
publisher = {{John Wiley & Sons Inc.}},
series = {{Annals of Neurology}},
title = {{Increased apolipoprotein E ε4 in epilepsy with senile plaques}},
url = {{http://dx.doi.org/10.1002/ana.410410317}},
doi = {{10.1002/ana.410410317}},
volume = {{41}},
year = {{1997}},
}