Karolina Kauppi
Karolinska Institutet
GeneGenome-wide association studyInternal medicineOncologySingle-nucleotide polymorphismPsychologyNeuroscienceCognitionGenetic associationBipolar disorderDiseaseFunctional magnetic resonance imagingDementiaCognitive declineLinkage disequilibriumGeneticsApolipoprotein EBioinformaticsComputational biologyMedicineCohortSchizophreniaBiology
40Publications
17H-index
1,352Citations
Publications 37
Newest
#1Koch E (Umeå University)
#2Lars NybergH-Index: 105
Last. Karolina KauppiH-Index: 17
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Polygenic risk for schizophrenia has been associated with lower cognitive ability and age-related cognitive change in healthy individuals. Despite well-established neuropsychological sex differences in schizophrenia patients, genetic studies on sex differences in schizophrenia in relation to cognitive phenotypes are scarce. Here, we investigated whether the effect of a polygenic risk score (PRS) for schizophrenia on childhood, midlife and late life cognitive function in healthy individuals is mo...
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Last. Pudas S
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#1Sara Pudas (Umeå University)H-Index: 14
#2Maria Josefsson (Umeå University)H-Index: 11
Last. Sofie Degerman (Umeå University)H-Index: 12
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Leukocyte telomere length (LTL) is a proposed biomarker for aging-related disorders, including cognitive decline and dementia. Long-term longitudinal studies measuring intra-individual changes in both LTL and cognitive outcomes are scarce, precluding strong conclusions about a potential aging-related relationship between LTL shortening and cognitive decline. This study investigated associations between baseline levels and longitudinal changes in LTL and memory performance across an up to 20-year...
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#1Lars Nyberg (Umeå University)H-Index: 105
Last. Rolf Adolfsson (Umeå University)H-Index: 80
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Abstract Individual differences in cognitive performance increase with advancing age, reflecting marked cognitive changes in some individuals along with little or no change in others. Genetic and lifestyle factors are assumed to influence cognitive performance in aging by affecting the magnitude and extent of age-related brain changes (i.e., brain maintenance or atrophy), as well as the ability to recruit compensatory processes. The purpose of this review is to present findings from the Betula s...
3 CitationsSource
#1Karolina Kauppi (KI: Karolinska Institutet)H-Index: 17
#2Michael Rönnlund (Umeå University)H-Index: 27
Last. Rolf Adolfsson (Umeå University)H-Index: 80
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Most people’s cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. Although APOE ɛ4 and genetic scores for late-onset Alzheimer’s disease (LOAD) have been related to cognitive decline during preclinical stages of dementia, there is limited knowledge concerning genetic factors implied in normal cognitive aging. In the present study, we examined three potential genetic predictors of age-related cognitive decline as follows:...
6 CitationsSource
#1Elise Koch (Umeå University)H-Index: 1
#2Brin Rosenthal (UCSD: University of California, San Diego)H-Index: 1
Last. Karolina Kauppi (KI: Karolinska Institutet)H-Index: 17
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Abstract Cognitive impairments constitute a core feature of schizophrenia, and a genetic overlap between schizophrenia and cognitive functioning in healthy individuals has been identified. However, due to the high polygenicity and complex genetic architecture of both traits, overlapping biological pathways have not yet been identified between schizophrenia and normal cognitive ability. Network medicine offers a framework to study underlying biological pathways through protein-protein interaction...
2 CitationsSource
#1Min-Tzu Lo (UCSD: University of California, San Diego)H-Index: 14
#2Karolina Kauppi (UCSD: University of California, San Diego)H-Index: 17
Last. Chi-Hua Chen (UCSD: University of California, San Diego)H-Index: 34
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Abstract The risk of APOE for Alzheimer's disease (AD) is modified by age. Beyond APOE, the polygenic architecture may also be heterogeneous across age. We aim to investigate age-related genetic heterogeneity of AD and identify genomic loci with differential effects across age. Stratified gene-based genome-wide association studies and polygenic variation analyses were performed in the younger (60–79 years, N = 14,895) and older (≥80 years, N = 6559) age-at-onset groups using Alzheimer's Disease ...
11 CitationsSource
#1Karolina KauppiH-Index: 17
#2Osman GaniH-Index: 2
Last. Chi-Hua ChenH-Index: 34
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#1Chin Hong Tan (NTU: Nanyang Technological University)H-Index: 15
#2Luke W. Bonham (UCSF: University of California, San Francisco)H-Index: 17
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: Mounting evidence indicates that the polygenic basis of late-onset Alzheimer's disease can be harnessed to identify individuals at greatest risk for cognitive decline. We have previously developed and validated a polygenic hazard score comprising of 31 single nucleotide polymorphisms for predicting Alzheimer's disease dementia age of onset. In this study, we examined whether polygenic hazard scores are associated with: (i) regional tracer uptake using amyloid PET; (ii) regional volume loss usi...
22 CitationsSource
#1Nilotpal Sanyal (UCSD: University of California, San Diego)H-Index: 6
#2Min-Tzu Lo (UCSD: University of California, San Diego)H-Index: 14
Last. Chi-Hua Chen (UCSD: University of California, San Diego)H-Index: 34
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Motivation: Multiple marker analysis of the genome-wide association study (GWAS) data has gained ample attention in recent years. However, because of the ultra high-dimensionality of GWAS data, suc ...
12 CitationsSource