Posterior cingulate cortex in familiar Alzheimer’s disease: A clinicopathological and brain imaging study
Risberg, Jarl LU ; Gustafson, Lars LU ; Brun, Arne LU ; Englund, Elisabet LU
and Ryding, Erik
LU
(2003)
The Thirty-First Annual International Neuropsychological Society Conference
In Journal of the International Neuropsychological Society
9.
p.174-174
- Abstract
- The degenerative process in Alzheimer´s disease (AD) follows a temporal and topographic pattern of early and accentuated involvement of temporal limbic, parietal and posterior cingulate cortices. We have studied a pedigree with four generations suffering from early onset AD linked to a presenilin-1 gene mutation. This family now contains 7 AD cases, neuropathologically confirmed in four cases of three generations. In all four cases the degeneration was most pronounced in the temporoparietal cortex, but also engaged central grey structures such as the claustrum, central thalamic and brain stem nuclei. There was a consistent and severe degeneration in posterior cingulate cortex in contrast to a compara¬tively spared anterior cingulum.... (More)
- The degenerative process in Alzheimer´s disease (AD) follows a temporal and topographic pattern of early and accentuated involvement of temporal limbic, parietal and posterior cingulate cortices. We have studied a pedigree with four generations suffering from early onset AD linked to a presenilin-1 gene mutation. This family now contains 7 AD cases, neuropathologically confirmed in four cases of three generations. In all four cases the degeneration was most pronounced in the temporoparietal cortex, but also engaged central grey structures such as the claustrum, central thalamic and brain stem nuclei. There was a consistent and severe degeneration in posterior cingulate cortex in contrast to a compara¬tively spared anterior cingulum. Regional cerebral blood flow (rCBF) was studied repeated¬ly with 133-xenon inhalation and SPECT methods. The rCBF measurements showed the typical cortical pathology of AD with bilateral decreases in temporoparietal and posterior cingulate cortices, accentuating over time and spreading anteriorly. There was a very good correspondence between clinical, neuroimaging and neuropathological features. Our findings indicate that posterior cingulum is a major locus for functional and structural vulnerability in both familial and sporadic forms of AD, something that might be used for diagnostic purposes together with possible posterior cingulate symptomatology. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/806313
- author
- Risberg, Jarl
LU
; Gustafson, Lars
LU
; Brun, Arne
LU
; Englund, Elisabet
LU
and Ryding, Erik
LU
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of the International Neuropsychological Society
- volume
- 9
- pages
- 174 - 174
- publisher
- Cambridge University Press
- conference name
- The Thirty-First Annual International Neuropsychological Society Conference
- conference location
- Honolulu, Hawaii, United States
- conference dates
- 2003-02-05 - 2003-02-08
- external identifiers
-
- scopus:0037310579
- ISSN
- 1355-6177
- DOI
- 10.1017/S1355617703920017
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Pathology, (Lund) (013030000), Clinical Neurophysiology (013013001), Department of Psychology (012010000), Department of Psychogeriatrics (013304000)
- id
- 78322b6b-1583-4b3d-94dc-1c4fad97d3ce (old id 806313)
- date added to LUP
- 2016-04-01 12:15:52
- date last changed
- 2022-01-30 03:59:13
@misc{78322b6b-1583-4b3d-94dc-1c4fad97d3ce,
abstract = {{The degenerative process in Alzheimer´s disease (AD) follows a temporal and topographic pattern of early and accentuated involvement of temporal limbic, parietal and posterior cingulate cortices. We have studied a pedigree with four generations suffering from early onset AD linked to a presenilin-1 gene mutation. This family now contains 7 AD cases, neuropathologically confirmed in four cases of three generations. In all four cases the degeneration was most pronounced in the temporoparietal cortex, but also engaged central grey structures such as the claustrum, central thalamic and brain stem nuclei. There was a consistent and severe degeneration in posterior cingulate cortex in contrast to a compara¬tively spared anterior cingulum. Regional cerebral blood flow (rCBF) was studied repeated¬ly with 133-xenon inhalation and SPECT methods. The rCBF measurements showed the typical cortical pathology of AD with bilateral decreases in temporoparietal and posterior cingulate cortices, accentuating over time and spreading anteriorly. There was a very good correspondence between clinical, neuroimaging and neuropathological features. Our findings indicate that posterior cingulum is a major locus for functional and structural vulnerability in both familial and sporadic forms of AD, something that might be used for diagnostic purposes together with possible posterior cingulate symptomatology.}},
author = {{Risberg, Jarl and Gustafson, Lars and Brun, Arne and Englund, Elisabet and Ryding, Erik}},
issn = {{1355-6177}},
language = {{eng}},
note = {{Conference Abstract}},
pages = {{174--174}},
publisher = {{Cambridge University Press}},
series = {{Journal of the International Neuropsychological Society}},
title = {{Posterior cingulate cortex in familiar Alzheimer’s disease: A clinicopathological and brain imaging study}},
url = {{http://dx.doi.org/10.1017/S1355617703920017}},
doi = {{10.1017/S1355617703920017}},
volume = {{9}},
year = {{2003}},
}