Profiles

Håkan Fischer, porträtt. Foto: Niklas Björling

Håkan Fischer

Professor, prefekt

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Arbetar vid Psykologiska institutionen
Telefon 08-16 23 57
E-post hakan.fischer@psychology.su.se
Besöksadress Frescati hagväg 14
Rum 136
Postadress Psykologiska institutionen 106 91 Stockholm

Om mig

Jag är professor i biologisk psykologi och sedan första augusti 2015 även prefekt här vid Psykologiska institutionen. Jag är också docent vid Karolinska Institutet och anknyten till Aging Research Center, Karolinska Institutet.

Jag började göra studier med funktionell hjärnavbildning 1993 och tog min doktorsexamen vid Uppsala Universitet 1998. Titeln på avhandlingen var Imaging fear and anxiety in the human brain. Mellan 1999 och 2001 genomförde jag min postdoktorala utbildning vid Harvard Medical School i Boston, USA. Efter detta fick jag en fyraårig anställning som forskarassistent från Vetenskapsrådet. Denna anställning lades vid Aging Research Center (ARC), Karolinska Institutet, där jag sedan fortsatte att arbeta som senior forskare, och från 2010 som vice sektionschef.

Jag handleder för närvarande sju doktorander. Två postdoktorer ingår också i forskargruppen. Sedan 2002 har jag regelbundet fått finansiering som huvudansvarig forskare för olika projekt främst från Vetenskapsrådet, men även från STINT, Riksbankens Jubileumsfond, och Konung Gustav V:s and Drottning Victorias Stiftelse.

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Undervisning

Jag har för närvarande bara enstaka föreläsningar på institutionen.

Forskning

Mitt primära forskningsområde är individuella skillnader i den neurobiologiska basen för emotionellt informationsprocessande, med särskild inriktning på åldrande och könsskillnader. Aktuella forskningslinjer här är:

  1. utvecklande av artificiell intelligens (AI) som korrekt kan avläsa och tolka emotionella uttryck i ansikten och röster tillsammans med forskare på Psykologiska institutionen, SU, University of Florida, Kungliga Tekniska högskolan och Research Institutes of Sweden (RISE).
  2. studiet av effekten av sömnbrist på emotionellt processande och dess neurobiologiska bas tillsammans med forskare vid Stressforskningsinstitutet och Karolinska Institutet,
  3. effekten av social stress på unga och äldre vuxna tillsammans med Stressforsningsinstitutet,
  4. effekten av oxytocin på socioemotionellt processande och dess neurobiologiska bas hos yngre och äldre personer tillsammans med forskare vid University of Florida och Göteborgs universitet,
  5. studiet av individuella skillnader i igenkänning av socioemotionell information samt träning av förmågan att detektera socioemotionell information, och slutligen
  6. emotionell reglering med fokus på habituering och extinktion hos yngre och äldre vuxna.

En annan forskningslinje är att studera emotionella processer och den neurala grunden för dessa hos psykiskt störda brottslingar med speciellt fokus på psykopati. Denna forskning gör jag i samarbete med sektionen för rättspsykiatri vid Karolinska Institutet, Huddinge, Institutionen för Klinisk Neurovetenskap vid Karolinska Institutet, Solna, samt Löwenströmska sjukhuset, Upplands Väsby.

Mitt vetenskapliga arbete har hittills resulterat i drygt 90 vetenskapliga artiklar som publicerats i internationella vetenskapliga tidskrifter. Mina publikationer har citerats mer än 6600 gånger i internationella vetenskapliga tidskrifter och jag har ett h-index på 37 (31 i Scopus) samt ett i10-index på 59. Jag har också tjänstgjort vid ett flertal halvtidskontroller och doktorsavhandlingskommittéer samt varit "reviewer" för ett flertal internationella vetenskapliga tidskrifter

I min forskning använder jag framför allt funktionell magnetresonanstomografi (fMRI), positronemissionstomografi (PET) och functional near-infrared optical brain imaging (FNIRS) för att studera hjärnans funktion, samt strukturell MRI (DTI och perfusion) för att studera hjärnans vit- och gråsubstans. Jag samarbetar både nationellt och internationellt med andra forskare och deltar i pågående projekt i Sverige, Tyskland och USA.

Läs mer om Fischers forskningslabb.

Läs mer på min sida på Research Gate.

Publikationer in press/accepted

Utöver de publicerade artiklarna nedan är följade artiklar under tryckning/accepterade:

1. Åkerstedt, T., Lekander, M., Nilsonne, G., Tamm, S.,  d’Onofrio, P., Kecklund, G., Fischer, H., Schwarz, J. (accepted). The effect of late night short sleep on polysomnography – the relation to age and gender. Journal of Sleep Research

2. Hovey, D., Henningsson, S., Cortes S., D., Bänziger, T., Zettergren, A., Melke, J., Fischer, H., Laukka, P., Westberg, L. (accepted).  Emotion recognition associated with polymorphism in oxytocinergic pathway gene ARNT2. Social Cognitive and Affective Neuroscience.

Publikationer

I urval från Stockholms universitets publikationsdatabas
  • 2017. Benjamin C. Holding (et al.). Sleep 40 (11)

    Objectives: Insufficient sleep has been associated with impaired recognition of facial emotions. However, previous studies have found inconsistent results, potentially stemming from the type of static picture task used. We therefore examined whether insufficient sleep was associated with decreased emotion recognition ability in two separate studies using a dynamic multimodal task.

    Methods: Study 1 used a cross-sectional design consisting of 291 participants with questionnaire measures assessing sleep duration and self-reported sleep quality for the previous night. Study 2 used an experimental design involving 181 participants where individuals were quasi-randomized into either a sleep-deprivation (N = 90) or a sleep-control (N = 91) condition. All participants from both studies were tested on the same forced-choice multimodal test of emotion recognition to assess the accuracy of emotion categorization.

    Results: Sleep duration, self-reported sleep quality (study 1), and sleep deprivation (study 2) did not predict overall emotion recognition accuracy or speed. Similarly, the responses to each of the twelve emotions tested showed no evidence of impaired recognition ability, apart from one positive association suggesting that greater self-reported sleep quality could predict more accurate recognition of disgust (study 1).

    Conclusions: The studies presented here involve considerably larger samples than previous studies and the results support the null hypotheses. Therefore, we suggest that the ability to accurately categorize the emotions of others is not associated with short-term sleep duration or sleep quality and is resilient to acute periods of insufficient sleep.

  • 2017. Sandra Tamm (et al.). Scientific Reports 7

    Age and sleep both affect emotional functioning. Since sleep patterns change over the lifespan, we investigated the effects of short sleep and age on empathic responses. In a randomized cross-over experimental design, healthy young and older volunteers (n = 47 aged 20–30 years and n = 39 aged 65–75 years) underwent functional magnetic resonance imaging (fMRI) after normal sleep or night sleep restricted to 3 hours. During fMRI, participants viewed pictures of needles pricking a hand (pain) or Q-tips touching a hand (control), a well-established paradigm to investigate empathy for pain. There was no main effect of sleep restriction on empathy. However, age and sleep interacted so that sleep restriction caused increased unpleasantness in older but not in young participants. Irrespective of sleep condition, older participants showed increased activity in angular gyrus, superior temporal sulcus and temporo-parietal junction compared to young. Speculatively, this could indicate that the older individuals adopted a more cognitive approach in response to others’ pain. Our findings suggest that caution in generalizability across age groups is needed in further studies of sleep on social cognition and emotion.

  • 2017. Gustav Nilsonne (et al.). Scientific Reports 7

    Sleep deprivation has been reported to affect intrinsic brain connectivity, notably reducing connectivity in the default mode network. Studies to date have however shown inconsistent effects, in many cases lacked monitoring of wakefulness, and largely included young participants. We investigated effects of sleep deprivation on intrinsic brain connectivity in young and older participants. Participants aged 20–30 (final n = 30) and 65–75 (final n = 23) years underwent partial sleep deprivation (3 h sleep) in a cross-over design, with two 8-minutes eyes-open resting state functional magnetic resonance imaging (fMRI) runs in each session, monitored by eye-tracking. We assessed intrinsic brain connectivity using independent components analysis (ICA) as well as seed-region analyses of functional connectivity, and also analysed global signal variability, regional homogeneity, and the amplitude of low-frequency fluctuations. Sleep deprivation caused increased global signal variability. Changes in investigated resting state networks and in regional homogeneity were not statistically significant. Younger participants had higher connectivity in most examined networks, as well as higher regional homogeneity in areas including anterior and posterior cingulate cortex. In conclusion, we found that sleep deprivation caused increased global signal variability, and we speculate that this may be caused by wake-state instability.

  • 2017. Johanna F. A. Schwarz (et al.). Journal of Sleep Research 26 (3), 277-287

    It is well known that the quantity and quality of physiological sleep changes across age. However, so far the effect of age on sleep microstructure has been mostly addressed in small samples. The current study examines the effect of age on several measures of sleep macro- and microstructure in 211 women (22–71 years old) of the ‘Sleep and Health in Women’ study for whom ambulatory polysomnography was registered. Older age was associated with significantly lower fast spindle (effect size f2 = 0.32) and K-complex density (f2 = 0.19) during N2 sleep, as well as slow-wave activity (log) in N3 sleep (f2 = 0.21). Moreover, total sleep time (f2 = 0.10), N3 sleep (min) (f2 = 0.10), rapid eye movement sleep (min) (f2 = 0.11) and sigma (log) (f2 = 0.05) and slow-wave activity (log) during non-rapid eye movement sleep (f2 = 0.09) were reduced, and N1 sleep (f2 = 0.03) was increased in older age. No significant effects of age were observed on slow spindle density, rapid eye movement density and beta power (log) during non-rapid eye movement sleep. In conclusion, effect sizes indicate that traditional sleep stage scoring may underestimate age-related changes in sleep.

  • 2017. Ninni Persson (et al.). Frontiers in Neuroscience 11

    Despite evidence of a fundamental role of DARPP-32 in integrating dopamine and glutamate signaling, studies examining gene coding for DARPP-32 in relation to neural and behavioral cor-relates in humans are scarce. Post mortem findings evidence genotype specific expressions of DARPP-32 in the dorsal frontal lobes. We therefore investigated the effects of genomic variation in DARPP-32 coding on frontal lobe volumes and episodic memory. Volumetric data from the dorsolateral (DLPFC), and visual cortices (VC) were obtained from 61 younger and older adults (♀54%). The major homozygote G, T or A genotypes in single nucleotide polymorphisms (SNPs: rs879606; rs907094; rs3764352), at the DARPP-32 regulating PPP1R1B gene influenced frontal gray matter volume and episodic memory (EM). Homozygous carriers of allelic variants with lower DARPP-32 expression had overall larger prefrontal volumes, in addition to greater EM recall accuracy. The SNPs did not influence VC volume. The genetic effects on DLPFC were greater in younger adults, and selective to this group for EM. Our findings suggest that genomic variation maps on to individual differences in frontal brain volumes, and cognitive functions. Larger DLPFC volumes were also related to better EM performance, suggesting that gene-related differences in frontal gray matter may contribute to individual differences in EM. These results need further replication from experimental and longitudinal reports to determine directions of causality.

  • 2017. Diana S. Cortes (et al.). PLoS ONE 12 (6)

    We investigated how memory for faces and voices (presented separately and in combination) varies as a function of sex and emotional expression (anger, disgust, fear, happiness, sadness, and neutral). At encoding, participants judged the expressed emotion of items in forced-choice tasks, followed by incidental Remember/Know recognition tasks. Results from 600 participants showed that accuracy (hits minus false alarms) was consistently higher for neutral compared to emotional items, whereas accuracy for specific emotions varied across the presentation modalities (i.e., faces, voices, and face-voice combinations). For the subjective sense of recollection (“remember” hits), neutral items received the highest hit rates only for faces, whereas for voices and face-voice combinations anger and fear expressions instead received the highest recollection rates. We also observed better accuracy for items by female expressers, and own-sex bias where female participants displayed memory advantage for female faces and face-voice combinations. Results further suggest that own-sex bias can be explained by recollection, rather than familiarity, rates. Overall, results show that memory for faces and voices may be influenced by the expressions that they carry, as well as by the sex of both items and participants. Emotion expressions may also enhance the subjective sense of recollection without enhancing memory accuracy.

  • 2017. Elmeri Syrjänen (et al.). Perception 46 (12), 1412-1426

    Disgust is a core emotion evolved to detect and avoid the ingestion of poisonous food as well as the contact with pathogens and other harmful agents. Previous research has shown that multisensory presentation of olfactory and visual information may strengthen the processing of disgust-relevant information. However, it is not known whether these findings extend to dynamic facial stimuli that changes from neutral to emotionally expressive, or if individual differences in trait body odor disgust may influence the processing of disgust-related information. In this preregistered study, we tested whether a classification of dynamic facial expressions as happy or disgusted, and an emotional evaluation of these facial expressions, would be affected by individual differences in body odor disgust sensitivity, and by exposure to a sweat-like, negatively valenced odor (valeric acid), as compared with a soap-like, positively valenced odor (lilac essence) or a no-odor control. Using Bayesian hypothesis testing, we found evidence that odors do not affect recognition of emotion in dynamic faces even when body odor disgust sensitivity was used as moderator. However, an exploratory analysis suggested that an unpleasant odor context may cause faster RTs for faces, independent of their emotional expression. Our results further our understanding of the scope and limits of odor effects on facial perception affect and suggest further studies should focus on reproducibility, specifying experimental circumstances where odor effects on facial expressions may be present versus absent.

  • 2017. Ninni Persson (et al.). Social Cognitive & Affective Neuroscience 12 (10), 1658-1667

    Dopaminergic pathways play a crucial role in reward processing, and advanced age can modulate its efficiency. DARPP-32 controls dopaminergic function and is a chemical nexus of reward processing. In 61 younger (20-30 years) and older adults (54% female) (65-74 years), we examined how blood-oxygen-level dependent (BOLD) activation to emotional faces, vary over genotypes at three single nucleotide polymorphism(SNPs), coding for DARPP-32 (rs879606; rs907094; 3764352). We also assessed age-magnification of DARPP-32 effects on BOLD activation. We found that major homozygote G, T or A genotypes, with higher cortical expression of DARPP-32, higher dopamine receptor efficacy, and greater bias toward positive cues, had increased functional connectivity in cortical-subcortical circuits in response to happy faces, engaging the dorsal prefrontal cortex (DLPFC), fusiform gyrus (FG) and the midbrain (MB). Local BOLD response to happy faces in FG, and MB was age dependent, so that older carriers of the major G, T or A alleles showed lesser activation than minor genotypes. These genetic variants of DARPP-32 did not modulate BOLD response to angry faces, or engagement of the inferior occipital gyrus, to happy or angry faces. Taken together our results lend support for a potential role of DARPP-32 genetic variants in neural response to potential reward triggering cues.

  • 2017. Daniel Lundqvist (et al.). Neuropsychology 31 (6), 605-612

    Objective: The literature on emotional processing in Parkinson's disease (PD) patients shows mixed results. This may be because of various methodological and/or patient-related differences, such as failing to adjust for cognitive functioning, depression, and/or mood. Method: In the current study, we tested PD patients and healthy controls (HCs) using emotional stimuli across a variety of tasks, including visual search, short-term memory (STM), categorical perception, and emotional stimulus rating. The PD and HC groups were matched on cognitive ability, depression, and mood. We also explored possible relationships between task results and antiparkinsonian treatment effects, as measured by levodopa equivalent dosages (LED), in the PD group. Results: The results show that PD patients use a larger emotional range compared with HCs when reporting their impression of emotional faces on rated emotional valence, arousal, and potency. The results also show that dopaminergic therapy was correlated with stimulus rating results such that PD patients with higher LED scores rated negative faces as less arousing, less negative, and less powerful. Finally, results also show that PD patients display a general slowing effect in the visual search tasks compared with HCs, indicating overall slowed responses. There were no group differences observed in the STM or categorical perception tasks. Conclusions: Our results indicate a relationship between emotional responses, PD, and dopaminergic therapy, in which PD per se is associated with stronger emotional responses, whereas LED levels are negatively correlated with the strength of emotional responses.

Visa alla publikationer av Håkan Fischer vid Stockholms universitet

Senast uppdaterad: 11 januari 2018

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