The importance of investigating Emotion Regulation (ER) may be self-evident, given that emotions have a substantial impact on our daily lives. ER encompasses set of processes that people go through in order to cultivate their feelings that arise at the moment and produce some response. Brain-imaging studies of ER have broadly focused on examining cognitive strategies, such as reappraisal, in order to understand underlying variables that contribute to the development of this particular process of emotions. The main focus in this paper was to summarize some of the observation done by functional Magnetic Resonance Imaging (fMRI) on neural processes underlying cognitive reappraisal. Furthermore, the paper will discuss some of these experiments that have been made through the last 15 years in the field where indications have been somewhat confusing when it comes to certain aspects of presented data, especially in comparison with other studies. Finally, a brief overview and some of the significant contributions, such as a process model of ER, to the field of ER have been presented and discussed. Cognitive reappraisal has been shown to effectively down-regulate subjective emotional experience. Even though many studies have been performed in measuring brain-activity when engaging in cognitive reappraisal, a unified and accepted agreement has yet not been found. In broader terms, brain-responses when engaging in cognitive reappraisal seem to operate in a particular manner where different parts of prefrontal and parietal cortex execute control over subcortical regions, such as amygdala.

Around 3-8% of all women in reproductive age suffer from premenstrual dysphoric disorder (PMDD) which disenables them to live an ordinary life during the luteal phase (premenstrual phase) of the menstrual cycle. Throughout the premenstrual phase these women experience emotional, cognitive and physiological changes. Hitherto, the etiology of this disorder is unknown. Some consider the source of this state as non-biological, claiming that PMDD is a social construction imbedded in gender roles, that suggests that women should not show aggressive behavior or depressive mood unless it is during the premenstrual stage. Contradictory, research made in cognitive neuroscience claim that the origin is biological. It is assumed that the increased symptoms in women with PMDD is a result from dysfunctional sensitivity for the progesterone metabolite allopregnanolone that has a receptor in the GABAA system, hence, producing an anxious effect from high levels of allopregnanolone instead of the expected sedative, soothing effects. Research suggest that structural and functional changes occur in brain areas such as the hippocampus, parahippocampus, amygdala, cerebellum as well as in brainderived neurotrophic factor which is important for brain plasticity, growth and survival of neurons. Cognitive behaviors such as anticipation for negative stimuli, working memory and lack of cognitive control also seem to be affected by PMDD. Nonetheless, the evidence is inconsistent, the area of research face multiple issues in regards to study designs, hence making generalization at this point difficult. In sum, this essay reviews recent studies conducted in neuroscience of cognitive changes in women with PMDD, with focus on functional, structural and behavioral changes between the phases of the cycle.

Perceptual load theory, together with the surround-suppression model suggest that stimulus surrounding attended stimuli is suppressed, especially if perceptual load is high. This study attempts to map surround-suppression using electroencephalography to measure neural activity related to suppression at four surrounding locations (2°, 3°, 4° and 6° from fixation). Color and orientation was used to manipulate load, and the effect of load was controlled through behavioral and neural measures using event related potentials. Our results demonstrate no statistically supported effect of load in behavioral data or SSVEP data, but unexplained increased neural amplitude of an early visual component (i.e. N1) in the (hypothesized) low load condition.

The phenomenon of empathy has been fascinating laymen and scholars for centuries and has recently been an important subject for cognitive neuroscientific study. Empathy refers to the ability to understand and share others’ emotions and a characteristic of this ability is the capacity to empathize with others in pain. This review intends to examine and read up on the current state of the field of the neural and behavioral mechanisms associated with empathy for pain. The neural underpinnings of the first-hand experience of pain have been shown to be activated in a person observing the suffering individual, and this similarity in brain activity has been referred to as shared networks. This phenomenon plays an important role in the study of empathy. However, different factors have been shown to influence empathy for pain, such as age, gender, affective link between observer and sufferer, as well as phylogenetic similarity. This thesis discusses these differences, as well as atypical aspects affecting the empathic ability such as synaesthesia for pain, psychopathy and Asperger’s disease. Further, empathy for pain can be modulated by the individual observing someone in pain. For example, caregivers often down-regulate their empathic response to patients in pain, possibly in order to focus on their treatment and assistance. Also, paying attention to harmful stimuli heightens the perception of pain; therefore, the painful experience can be less remarkable when focusing on something else. The effect of empathy from others directed to oneself when suffering is discussed, as well as the consistency and limitations of presented research.

Alzheimer’s Disease is the most common form of dementia, affecting 48 million people worldwide. Despite this fact, only 45% of the patients have received the diagnose. The reason behind this is the fact that the cause of the disease is still unclear. Several hypotheses have been suggested, with main focus in the imbalance between the production and the clearance of Αβ in the brain (formation of plaques) or hyperphosphorylation of the tau protein (formation of tangles). In order to have a better understanding of what is actually happening in the brain, more biomarkers need to be developed. Keeping this in mind, we tried to develop a method to monitor the protein levels of SAP in the brain. SAP is a glycoprotein, normally produced by the liver in acute phase immune responses. SAP has been correlated with AD in the 1980s and quite recently it has been shown that SAP is elevated in AD patients, but not in individuals with plaques and no dementia. For this reason, we developed a mass spectrometry based targeted quantification method for monitoring SAP in the brain, as well as C9, a blood contamination reference protein. Our method is robust enough to be further used in large studies, in order to investigate the role of SAP in AD.

The influence of facial mimicry and emotional congruence on emotional information processing has previously only been studied in isolation. In the current study their influence on the ability to detect deception will be investigated. In order to recognize the emotional states of others one mimics their emotional facial expression, and being in a congruent emotional state as a person or an emotional message enables faster processing of emotional information. Can emotional congruence between the receiver’s emotional state and a message told affect participants’ ability to detect deception when judging whether a person at a video recording is telling the truth or not? How does emotional congruence affect participants’ speed and confidence when making these judgments? The results showed that participants reported higher confidence but slower response times when making an accurate judgment in the congruent scenario, when compared to the incongruent scenario, but did not perform better than what could be expected by chance in detecting deception. Consequently, emotional congruence had an impact, not on participants’ performance in detecting deception, but only on their meta-cognitive evaluations of their judgments, but confidence rating did not seem to be an indicator of accuracy. In future research the design can be used in order to investigate other potential aspects, such as emotional empathy and other types of emotional congruence, and their influence on the ability to detect deception.

The expansion of the voltage-gated calcium channel alpha 1 subunit families (CACNA1) of L and N types was investigated by combining phylogenetic analyses (neighbour-joining and maximum likelihood) with chromosomal data. Neighbouring gene families were analysed to see if the chromosomal regions duplicated through whole genome doublings in vertebrates. Results show that both types of CACNA1 expanded in two ancient whole genome duplications as parts of larger genomic regions. Many gene families in these regions obtained copies in an additional teleost-specific genome duplication. This diversification of CACNA1 genes probably contributed to evolutionary innovations in nervous system function.

This literature review explores human mirror neurons from several angles. First it retells mirror neuron history, from the initial discovery in the macaque monkey research through to the experiments determining if there is a human brain homologue. Then the merits of two opposing evolutionary views – mirror neurons as an adaptation or an association, here referring to an adaptation’s byproduct – are discussed. Lastly the autistic mirror neuron dysfunction hypothesis – stating that a faulty mirror neuron system is at the basis of autistic behavioral patterns – is examined for its validity but ultimately found lacking and in need of further development.

Stress är i sig inte farlig om den inte blir långvarig och konstant, den här rapporten har tittat på vilka effekter och eventuella konsekvenser stress har på de fysiologiska och kognitiva systemen hos människan. En långvarig aktivering av HPA-axeln, vilken kan kallas prestations/stressaxeln, leder bland annat till kroniskt förhöjda kortisolnivåer vilket har negativa effekter för hälsan. Strukturer i hjärnan vilka ofta kopplas till stressrelaterade sjukdomar är hippocampus och prefrontala kortex. De konsekvenserna som kan följa på långvarig stress är kognitiva nedsättningar och skador på bland annat hippocampus, brister i immunförsvaret, hjärt- och kärlsjukdomar, ångest, kroniskt utmattningssyndrom, mag- och tarmbesvär samt depression. I rapporten visas att stress har stora negativa konsekvenser på individnivå både gällande kognitiva funktioner, så som minne, och även på det fysiologiska systemet. Det finns åtgärder att använda för att reducera upplevelsen av stress samt de negativa effekterna av stress, så som fysisk aktivitet, mindfulness meditation och muskulär avslappning.

Tinnitus is a phantom auditory perception characterized by a ringing sound in either one or both ears. It is a common disorder most often associated with hearing loss and can have a severe impact on a person's quality of life. There is currently no cure and no efficient therapeutic options. There is little known about the neural mechanisms underlying the generation of tinnitus but a better understanding of its neural basis could greatly benefit the development of efficient treatment methods. This literature study aims to explore the neural mechanisms of tinnitus in terms of generation, perpetuation, and perception. Cochlear dysfunction, changes in neuronal firing rates and oscillatory properties, hyperactivity, lack of inhibitory activity and plasticity in auditory-limbic structures have been associated with tinnitus and may be a part of a crossmodal network involved in generating, perpetuating and perceiving tinnitus, through maladaptive CNS plasticity. New developing treatment methods aim to modulate and re-route tinnitus-related plasticity, however, this leads to treatment difficulties due to the crossmodal nature of the tinnitus pathophysiology. These difficulties will be further examined in the discussion.