Neural substrates of cognitive and behavioral deficits in atypical Alzheimer's disease

Details

Serval ID
serval:BIB_F204E9D19424
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Neural substrates of cognitive and behavioral deficits in atypical Alzheimer's disease
Journal
Brain Research Reviews
Author(s)
Gunten Armin von, Bouras Constantin, Kövari Enikö, Giannakopoulos Panteleimon, Hof Patrick R.
ISSN
0165-0173
Publication state
Published
Issued date
2006
Peer-reviewed
Oui
Volume
51
Number
2
Pages
176-211
Language
english
Notes
SAPHIRID:61676
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a progressive cognitive decline that typically affects first memory and later executive functions, language, and visuospatial skills. This sequence of cognitive deterioration is thought to reflect the progressive invasion of the cerebral cortex by the two major pathological hallmarks of AD, neurofibrillary tangles (NFT) and senile plaques (SP), as well as degree of neuronal and synaptic loss. In atypical AD, prominent and early deficits are found in language, motor abilities, frontal and executive capacities, or visuospatial skills. These atypical clinical features are associated with an unusual pattern of NFT or SP formation that predominantly involves cortical areas usually spared in the course of the degenerative process. In an attempt to classify this highly heterogeneous subgroup, the present article provides an overview of clinicopathological analyses in patients with atypical progression of AD symptomatology with special reference to the relationship between specific cognitive and behavioral deficits and hierarchical patterns of AD lesion distribution within the cerebral cortex. On the basis of these representative examples of a cortical circuit-based approach to explore the mechanisms giving rise to AD neuropsychological expression, we also critically discuss the possibility to develop a matrix linking clinical presentations to degeneration of forward and backward long corticocortical pathways in this disorder. [References: 280]
Pubmed
Web of science
Create date
10/03/2008 12:04
Last modification date
20/08/2019 17:19
Usage data