A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Early detection of Alzheimer disease: ¹¹C-PiB PET in twins discordant for cognitive impairment
Tekijät: Scheinin NM, Aalto S, Kaprio J, Koskenvuo M, Räihä I, Rokka J, Hinkka-Yli-Salomäki S, Rinne JO
Julkaisuvuosi: 2011
Journal: Neurology
Tietokannassa oleva lehden nimi: Neurology
Lehden akronyymi: Neurology
Vuosikerta: 77
Numero: 5
Aloitussivu: 453
Lopetussivu: 60
Sivujen määrä: 8
ISSN: 0028-3878
eISSN: 1526-632X
DOI: https://doi.org/10.1212/WNL.0b013e318225118e
Tiivistelmä
The aim of this study was to investigate whether cognitively preserved monozygotic or dizygotic cotwins of persons with Alzheimer disease (AD) exhibit increased brain amyloid accumulation.\nWe performed a cross-sectional carbon-11 labeled 2-(4'-methylaminophenyl)-6-hydroxybenzothiazole ((11)C)-Pittsburgh compound B (PiB) PET study on 9 monozygotic and 8 dizygotic twin pairs discordant for cognitive impairment as well as on 9 healthy elderly control subjects. (11)C-PiB uptake was analyzed with Statistical Parametric Mapping and with region of interest analysis with the region-to-cerebellum ratio as a measure of tracer uptake.\nCognitively preserved monozygotic cotwins of cognitively impaired probands had increased cortical (11)C-PiB uptake (117%-121% of control mean) in their temporal and parietal cortices and the posterior cingulate. Cognitively preserved dizygotic subjects did not differ from the controls. Further, the cognitively preserved monozygotic subjects showed similar (11)C-PiB uptake patterns as their cognitively impaired cotwins. The cognitively impaired subjects (monozygotic and dizygotic individuals combined) showed typical Alzheimer-like patterns of (11)C-PiB uptake.\nGenetic factors appear to influence the development of Alzheimer-like β-amyloid plaque pathology. The dissociation between cognitive impairment and brain β-amyloidosis in monozygotic twins implies that there may be important environmental/acquired factors that modulate the relationship between brain amyloidosis and neurodegeneration. AD may be detectable in high-risk individuals in its presymptomatic stage with (11)C-PiB PET, but clinical follow-up will be needed to confirm this.\nOBJECTIVE\nMETHODS\nRESULTS\nCONCLUSIONS
The aim of this study was to investigate whether cognitively preserved monozygotic or dizygotic cotwins of persons with Alzheimer disease (AD) exhibit increased brain amyloid accumulation.\nWe performed a cross-sectional carbon-11 labeled 2-(4'-methylaminophenyl)-6-hydroxybenzothiazole ((11)C)-Pittsburgh compound B (PiB) PET study on 9 monozygotic and 8 dizygotic twin pairs discordant for cognitive impairment as well as on 9 healthy elderly control subjects. (11)C-PiB uptake was analyzed with Statistical Parametric Mapping and with region of interest analysis with the region-to-cerebellum ratio as a measure of tracer uptake.\nCognitively preserved monozygotic cotwins of cognitively impaired probands had increased cortical (11)C-PiB uptake (117%-121% of control mean) in their temporal and parietal cortices and the posterior cingulate. Cognitively preserved dizygotic subjects did not differ from the controls. Further, the cognitively preserved monozygotic subjects showed similar (11)C-PiB uptake patterns as their cognitively impaired cotwins. The cognitively impaired subjects (monozygotic and dizygotic individuals combined) showed typical Alzheimer-like patterns of (11)C-PiB uptake.\nGenetic factors appear to influence the development of Alzheimer-like β-amyloid plaque pathology. The dissociation between cognitive impairment and brain β-amyloidosis in monozygotic twins implies that there may be important environmental/acquired factors that modulate the relationship between brain amyloidosis and neurodegeneration. AD may be detectable in high-risk individuals in its presymptomatic stage with (11)C-PiB PET, but clinical follow-up will be needed to confirm this.\nOBJECTIVE\nMETHODS\nRESULTS\nCONCLUSIONS
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