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KIBRA polymorphism is related to enhanced memory and elevated hippocampal processing
Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Fysiologi. Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
Stockholm University.
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.ORCID-id: 0000-0002-8114-7615
Gothenburg University.
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2011 (Engelska)Ingår i: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 31, nr 40, s. 14218-14222Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Several studies have linked the KIBRA rs17070145 T polymorphism to superior episodic memory in healthy humans. One study investigated the effect of KIBRA on brain activation patterns (Papassotiropoulos et al., 2006) and observed increased hippocampal activation in noncarriers of the T allele during retrieval. Noncarriers were interpreted to need more hippocampal activation to reach the same performance level as T carriers. Using large behavioral (N = 2230) and fMRI (N = 83) samples, we replicated the KIBRA effect on episodic memory performance, but found increased hippocampal activation in T carriers during episodic retrieval. There was no evidence of compensatory brain activation in noncarriers within the hippocampal region. In the main fMRI sample, T carriers performed better than noncarriers during scanning but, importantly, the difference in hippocampus activation remained after post hoc matching according to performance, sex, and age (N = 64). These findings link enhanced memory performance in KIBRA T allele carriers to elevated hippocampal functioning, rather than to neural compensation in noncarriers.

Ort, förlag, år, upplaga, sidor
Society for Neuroscience , 2011. Vol. 31, nr 40, s. 14218-14222
Nationell ämneskategori
Neurovetenskaper
Identifikatorer
URN: urn:nbn:se:umu:diva-48524DOI: 10.1523/JNEUROSCI.3292-11.2011ISI: 000295805500018PubMedID: 21976506OAI: oai:DiVA.org:umu-48524DiVA, id: diva2:450434
Forskningsfinansiär
VetenskapsrådetKnut och Alice Wallenbergs StiftelseTorsten Söderbergs stiftelseRagnar Söderbergs stiftelseHjärnfondenTillgänglig från: 2011-10-20 Skapad: 2011-10-20 Senast uppdaterad: 2019-01-30Bibliografiskt granskad
Ingår i avhandling
1. Genes to remember: imaging genetics of hippocampus-based memory functions
Öppna denna publikation i ny flik eller fönster >>Genes to remember: imaging genetics of hippocampus-based memory functions
2013 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

In the field of imaging genetics, brain function and structure are used as intermediate phenotypes between genes and cognition/diseases to validate and extend findings from behavioral genetics. In this thesis, three of the strongest candidate genes for episodic memory, KIBRA, BDNF, and APOE, were examined in relation to memory performance and hippocampal/parahippocampal fMRI blood-oxygen level-dependent (BOLD) signal. A common T allele in the KIBRA gene was previously associated with superior memory, and increased hippocampal activation was observed in noncarriers of the T allele which was interpreted as reflecting compensatory recruitment. The results from the first study revealed that both memory performance and hippocampal activation at retrieval was higher in T allele carriers (study I). The BDNF 66Met and APOE ε4 alleles have previously been associated with poorer memory performance, but their relation to brain activation has been inconsistent with reports of both increased and decreased regional brain activation relative to noncarriers. Here, decreased hippocampal/parahippocampal activation was observed in carriers of BDNF 66Met (study II) as well as APOE ε4 (study III) during memory encoding. In addition, there was an additive gene-gene effect of APOE and BDNF on hippocampal and parahippocampal activation (study III). Collectively, the results from these studies on KIBRA, BDNF, and APOE converge on higher medial temporal lobe activation for carriers of a high-memory associated allele, relative to carriers of a low-memory associated allele. In addition, the observed additive effect of APOE and BDNF demonstrate that a larger amount of variance in BOLD signal change can be explained by considering the combined effect of more than one genetic polymorphism. These imaging genetics findings support and extend previous knowledge from behavioral genetics on the role of these memory-related genes.

Ort, förlag, år, upplaga, sidor
Umeå: Umeå Universitet, 2013. s. 84
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1580
Nyckelord
Imaging genetics, fMRI, Episodic memory, SNP, KIBRA, BDNF, APOE, Hippocampus, Parahippocampus
Nationell ämneskategori
Neurovetenskaper
Identifikatorer
urn:nbn:se:umu:diva-71141 (URN)978-91-7459-598-7 (ISBN)978-91-7459-597-0 (ISBN)
Disputation
2013-06-14, BiA 201, Biologihuset, Umeå universitet, Umeå, 10:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2013-05-24 Skapad: 2013-05-20 Senast uppdaterad: 2018-06-08Bibliografiskt granskad

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FysiologiUmeå centrum för funktionell hjärnavbildning (UFBI)PsykiatriDiagnostisk radiologi
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