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

von Gunten, Armin; Bouras, Constantin; Kövari, Enikö; Giannakopoulos, Panteleimon; Hof, Patrick R.

doi:10.1016/j.brainresrev.2005.11.003

Cited by 75Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

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

von Gunten, Armin, Bouras, Constantin, Kövari, Enikö, Giannakopoulos, Panteleimon, Hof, Patrick R.·2006·Brain Research Reviews

DOI 10.1016/j.brainresrev.2005.11.003

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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.

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From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [7]

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Background
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Authors: von Gunten, A., Bouras, C., Kövari, E., Giannakopoulos, P., & Hof, P. R.
Affiliations: University Hospital of Geneva (CH)
Icahn School of Medicine at Mount Sinai (US)
ORCID: Hof, Patrick R.
Venue: Brain Research Reviews
Publisher: Elsevier BV
Published: 2006-08
Volume: 51
Issue: 2
Pages: 176-211
ISSN: 0165-0173 (ISSN-L)
DOI: 10.1016/j.brainresrev.2005.11.003
OpenAlex: W2088923332
Cited by: 75
References: 289
Citations by year: 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2020: 3 · 2019: 4 · 2018: 1 · 2017: 5 · 2016: 1 · 2015: 2 · 2014: 7 · 2013: 7 · 2012: 6
FWCI: 3.19
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Brain Research Reviews (publishedVersion)
PubMed (publishedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion)
Funders: National Institutes of Health
National Institute on Aging (AG-02219, AG 05138, P50AG005138, P01AG002219)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: atypical Alzheimer's disease, neurofibrillary tangles, amyloid plaques, cognitive impairment, behavioral deficits, language impairment, visuospatial deficits, executive dysfunction, motor impairment, cortico-cortical pathways, clinicopathological correlation
MeSH terms: Adult, Aged, Alzheimer Disease, Behavioral Symptoms, Cerebral Cortex, Cognition Disorders, Female, Humans, Male, Middle Aged, Models, Neurological, Neural Pathways, Neurofibrillary Tangles, Age of Onset, Disease Progression, Plaque, Amyloid

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

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