Literature DB >> 17698712

Dissociation of neuropathologic findings and cognition: case report of an apolipoprotein E epsilon2/epsilon2 genotype.

Daniel J Berlau1, Kristin Kahle-Wrobleski, Elizabeth Head, Matthew Goodus, Ronald Kim, Claudia Kawas.   

Abstract

BACKGROUND: The apolipoprotein E (APOE) epsilon2 allele has been suggested as having a protective effect and delaying the age at onset of Alzheimer disease.
OBJECTIVE: To describe a dissociation between neuropathologic findings with normal cognition in a woman with severe Alzheimer disease with the APOE epsilon2/epsilon2 genotype.
DESIGN: Case report from a community-based prospective study of persons 90 years or older (The 90+ Study). PARTICIPANT: A 92-year-old woman without dementia with the APOE epsilon2/epsilon2 genotype who lived independently without significant cognitive or functional loss and was a participant in The 90+ Study. She died in December 2004, and postmortem examination of her brain was performed. INTERVENTION: Neurologic examination and a battery of neuropsychological tests were performed 6 months and 1 month before death. Neuropathologic examination included Braak and Braak staging for senile plaques and neurofibrillary tangles.
RESULTS: Neuropathologic examination of the brain revealed advanced senile plaque and neurofibrillary tangle disease consistent with a high likelihood of Alzheimer disease. At clinical evaluation, the participant demonstrated no dementia and only mild cognitive deficits.
CONCLUSIONS: The APOE genotype may have contributed to maintenance of cognition despite advanced neuropathologic findings of Alzheimer disease. This case suggests that the APOE epsilon2 isoform may have a protective effect against cognitive decline in Alzheimer disease that may be independent from senile plaques and neurofibrillary tangles.

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Year:  2007        PMID: 17698712      PMCID: PMC3378248          DOI: 10.1001/archneur.64.8.1193

Source DB:  PubMed          Journal:  Arch Neurol        ISSN: 0003-9942


  21 in total

1.  Neuropsychological data in nondemented oldest old: the 90+ Study.

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3.  Prevalence of chronic disease and health practices in a retirement community.

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5.  Clinico-pathologic studies in dementia: nondemented subjects with pathologically confirmed Alzheimer's disease.

Authors:  H Crystal; D Dickson; P Fuld; D Masur; R Scott; M Mehler; J Masdeu; C Kawas; M Aronson; L Wolfson
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6.  Frequency of the apolipoprotein E epsilon 2 allele is diminished in sporadic Alzheimer disease.

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7.  Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease.

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10.  Clinical, pathological, and neurochemical changes in dementia: a subgroup with preserved mental status and numerous neocortical plaques.

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  21 in total

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2.  Probable early-onset Alzheimer's disease in an apolipoprotein E2 homozygote.

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3.  Neuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease.

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6.  A nonhuman primate model of Alzheimer's disease generated by intracranial injection of amyloid-β42 and thiorphan.

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7.  Apolipoprotein E highly correlates with AbetaPP- and tau-related markers in human cerebrospinal fluid.

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9.  Neocortical β-amyloid area is associated with dementia and APOE in the oldest-old.

Authors:  Daniel J Berlau; María M Corrada; John L Robinson; Felix Geser; Steven E Arnold; Virginia M-Y Lee; Claudia H Kawas; John Q Trojanowski
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Review 10.  Neuropathology and cognitive impairment in Alzheimer disease: a complex but coherent relationship.

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