TY  - JOUR
AU  - Eijndhoven, P.F. van
AU  - Wingen, G.A. van
AU  - Fernandez, G.S.E.
AU  - Rijpkema, M.J.P.
AU  - Pop-Purceleanu, M.
AU  - Verkes, R.J.
AU  - Buitelaar, J.K.
AU  - Tendolkar, I.
PY  - 2013
UR  - https://hdl.handle.net/2066/115407
AB  - BACKGROUND: Patients with major depressive disorder (MDD) display impairments in recollection, which have been explained by both hippocampal and prefrontal dysfunction. Here, we used an event-related fMRI design, to dissociate hippocampal and prefrontal contributions to the neural processes involved in recollection success and recollection attempt early in the course of MDD. METHODS: To disentangle state- and trait-effects of depression, we included 20 medication-naive patients with a first depressive episode, 20 medication-free patients recovered from a first episode, and 20 matched, healthy controls in an event-related fMRI study using a source recollection paradigm. RESULTS: Group comparisons revealed that during the acute state of depression there is an increase in left prefrontal activity related to recollection attempt, while there were no differences in neural correlates of successful recollection. CONCLUSIONS: Our results indicate that in the early course of depression, depressive state is associated with increased left prefrontal activation during the attempt to recollect source information suggesting an increased need for executive control during recollection in MDD. In this sample of first-episode MDD patients we found no evidence for hippocampal dysfunction.
TI  - Neural basis of recollection in first-episode major depression
EP  - 294
SN  - 1065-9471
IS  - iss. 2
SP  - 283
JF  - Human Brain Mapping
VL  - vol. 34
DO  - https://doi.org/10.1002/hbm.21439
ER  - 
TY  - JOUR
AU  - Gerritsen, L.
AU  - Rijpkema, M.J.P.
AU  - Oostrom, I.I.H. van
AU  - Buitelaar, J.K.
AU  - Franke, B.
AU  - Fernandez, G.S.E.
AU  - Tendolkar, I.
PY  - 2012
UR  - https://hdl.handle.net/2066/109103
AB  - Background. Negative memory bias is thought to be one of the main cognitive risk and maintenance factors for depression, but its neural substrates are largely unknown. Here, we studied whether memory bias is related to amygdala and hippocampal volume, two structures that are critical for emotional memory processes and that show consistent volume alterations in depression. Method. Structural magnetic resonance imaging (MRI) was carried out in 272 healthy participants (62% female, 18-50 years old). All images were acquired on 1.5 T Siemens MRI scanners. Automatic segmentation of amygdala and hippocampus was performed using the FIRST module of FSL. Negative memory bias was assessed by the self-referent encoding/evaluation test. Results. Negative memory bias was associated with larger amygdala (p = 0.042) and smaller hippocampal (p = 0.029) volumes. In additional analyses, we found that, compared with the associations found with hippocampus and amygdala volume separately, a stronger association was found between negative memory bias and the ratio of amygdala: hippocampus volume (p = 0.021). Conclusions. In non-depressed subjects we found that larger amygdala and smaller hippocampal volumes are associated with negative memory bias. This suggests that an increased amygdala: hippocampus volume ratio plays a role in cognitive vulnerability often seen in individuals with high risk for depression and that these structural brain differences may pre-date the onset of depression. Received 23 January 2011; Revised 15 June 2011; Accepted 15 June 2011; First published online 11 July 2011
TI  - Amygdala to hippocampal volume ratio is associated with negative memory bias in healthy subjects
EP  - 343
SN  - 0033-2917
IS  - iss. 2
SP  - 335
JF  - Psychological Medicine
VL  - vol. 42
DO  - https://doi.org/10.1017/S003329171100122X
ER  - 
TY  - JOUR
AU  - Gerritsen, L.
AU  - Tendolkar, I.
AU  - Franke, B.
AU  - Arias Vasquez, A.
AU  - Kooijman, S.
AU  - Buitelaar, J.K.
AU  - Fernandez, G.S.E.
AU  - Rijpkema, M.J.P.
PY  - 2012
UR  - https://hdl.handle.net/2066/110356
AB  - According to the neurotrophic hypothesis of depression, stress can lead to brain atrophy by modifying brain-derived neurotrophic factor (BDNF) levels. Given that BDNF secretion is affected by a common polymorphism (rs6265, Val66Met), which also is associated with depression, we investigated whether this polymorphism modifies the effect of childhood adversity (CA) on local gray matter (GM) volume in depression-relevant brain regions, using data from two large cohorts of healthy subjects. We included 568 healthy volunteers (aged 18-50 years, 63% female) in our study, for whom complete data were available, with magnetic resonance imaging data at 1.5 Tesla (N=275) or 3 Tesla (N=293). We used a whole brain optimized voxel-based morphometry (VBM) approach assessing genotype-dependent GM differences, with focus on the amygdala, hippocampus and medial prefrontal cortex (PFC; including anterior cingulate cortex (ACC) and orbitomedial PFC). CA was assessed using a validated questionnaire. In both cohorts, we found that BDNF methionine (Met)-allele carriers with a history of CA had significantly less GM in subgenual ACC (P<0.05) compared with Met-allele carriers without CA and Val/Val homozygotes with CA. No differences were found in hippocampus, amygdala and orbitomedial PFC. On the basis of our findings, we conclude that BDNF Met-allele carriers are particularly sensitive to CA. Given the key role of the subgenual ACC in emotion regulation, this finding provides an important mechanistic link between stress and BDNF on one hand and mood impairments on the other hand.
TI  - BDNF Val66Met genotype modulates the effect of childhood adversity on subgenual anterior cingulate cortex volume in healthy subjects.
EP  - 603
SN  - 1359-4184
IS  - iss. 6
SP  - 597
JF  - Molecular Psychiatry
VL  - vol. 17
N1  - 1 juni 2012
DO  - https://doi.org/10.1038/mp.2011.51
ER  - 
TY  - JOUR
AU  - Wingen, G.A. van
AU  - Rijpkema, M.J.P.
AU  - Franke, B.
AU  - Eijndhoven, P.F.P. van
AU  - Tendolkar, I.
AU  - Verkes, R.J.
AU  - Buitelaar, J.K.
AU  - Fernandez, G.S.E.
PY  - 2010
UR  - https://hdl.handle.net/2066/88956
AB  - Brain-derived neurotrophic factor (BDNF) is involved in memory and the pathophysiology of various neuropsychiatric disorders. A single nucleotide polymorphism in the human BDNF gene (Val66Met) affects memory, and influences Alzheimer's disease and depression vulnerability in a sex-specific manner. Recent animal studies suggest that BDNF mediates memory for emotional experiences in the amygdala, but it is currently unknown whether BDNF Val66Met influences memory processing in the amygdala. Here, we investigated its effect on the successful encoding and recognition of biologically salient stimuli. Forty-seven healthy volunteers memorized and recognized faces while their brain activity was measured with event-related functional MRI. No significant differences in memory performance were observed between Val homozygotes and Met allele carriers. The imaging results demonstrated BDNF genotype x sex interactions in the amygdala during memory formation, and in the prefrontal cortex and posterior cingulate cortex during memory retrieval. Subsequent tests showed a larger contribution of these brain regions to successful encoding and retrieval in male Met allele carriers than male Val homozygotes, whereas no significant differences were observed in females. These results provide preliminary evidence that the BDNF Val66Met polymorphism influences specific mnemonic operations underlying encoding and retrieval of salient stimuli, and suggest less efficient memory processing in male Met allele carriers. Furthermore, the sex-specific genotype effects may contribute to sex-specific effects of BDNF Val66Met on depression vulnerability.
TI  - The brain-derived neurotrophic factor Val66Met polymorphism affects memory formation and retrieval of biologically salient stimuli.
EP  - 1218
SN  - 1053-8119
IS  - iss. 3
SP  - 1212
JF  - NeuroImage
VL  - vol. 50
DO  - https://doi.org/10.1016/j.neuroimage.2010.01.058
ER  - 
TY  - JOUR
AU  - Wingen, G.A. van
AU  - Rijpkema, M.J.P.
AU  - Franke, B.
AU  - Eijndhoven, P.F.P. van
AU  - Tendolkar, I.
AU  - Verkes, R.J.
AU  - Buitelaar, J.K.
AU  - Fernandez, G.S.E.
PY  - 2010
UR  - https://hdl.handle.net/2066/88955
TI  - The brain-derived neurotrophic factor Val66Met polymorphism affects memory formation and retrieval of biologically salient stimuli
EP  - 1218
SN  - 1053-8119
IS  - iss. 3
SP  - 1212
JF  - NeuroImage
VL  - vol. 50
DO  - https://doi.org/10.1016/j.neuroimage.2010.01.058
ER  - 
TY  - JOUR
AU  - Eijndhoven, P.F.P. van
AU  - Wingen, G.A. van
AU  - Oijen, K. van
AU  - Rijpkema, M.J.P.
AU  - Goraj, B.M.
AU  - Verkes, R.J.
AU  - Oude Voshaar, R.C.
AU  - Fernandez, G.S.E.
AU  - Buitelaar, J.K.
AU  - Tendolkar, I.
PY  - 2009
UR  - https://hdl.handle.net/2066/77468
AB  - BACKGROUND: The amygdala and hippocampus play a key role in the neural circuitry mediating depression. It remains unclear how much structural and functional changes of amygdala and hippocampus reflect the acute state of depression or an underlying neurobiological trait marker of depression. METHODS: High-resolution anatomical images were acquired in 20 medication-naive major depressive disorder (MDD) patients with a current first episode, 20 medication-free patients recovered from a first episode of MDD, and 20 healthy control subjects that were matched for age, gender, and level of education. Manual volumetry of amygdala and hippocampus was performed on coronal images. Volumetric measurements of brain volume and intracranial volume were acquired with automatic segmentation procedures. RESULTS: Both amygdalae were significantly enlarged in currently depressed patients, whereas there was no significant difference between recovered patients and control subjects. The amygdala enlargement correlated positively with the severity of depressive state but with no other clinical or neuropsychological variable. The hippocampal volume did not differ between groups. CONCLUSIONS: A state related increase of amygdala volume can be detected early in the course of MDD. Neurotoxic effects might account for the fact that state-related amygdala enlargement has not been found in recurrent depression with relative long illness duration.
TI  - Amygdala volume marks the acute state in the early course of depression.
EP  - 818
SN  - 0006-3223
IS  - iss. 9
SP  - 812
JF  - Biological Psychiatry
VL  - vol. 65
DO  - https://doi.org/10.1016/j.biopsych.2008.10.027
ER  -