Salience and default mode network coupling predicts cognition in aging and Parkinson’s disease

OBJECTIVES: Cognitive impairment is common in Parkinson’s disease (PD). Three neurocognitive networks support efficient cognition: the salience network, the default mode network, and the central executive network. The salience network is thought to switch between activating and deactivating the default mode and central executive networks. Anti-correlated interactions between the salience and default mode networks in particular are necessary for efficient cognition. Our previous work demonstrated altered functional coupling between the neurocognitive networks in non-demented individuals with PD compared to age-matched control participants. Here, we aim to identify associations between cognition and functional coupling between these neurocognitive networks in the same group of participants. METHODS: We investigated the extent to which intrinsic functional coupling among these neurocognitive networks is related to cognitive performance across three neuropsychological domains: executive functioning, psychomotor speed, and verbal memory. Twenty-four non-demented individuals with mild to moderate PD and 20 control participants were scanned at rest and evaluated on three neuropsychological domains. RESULTS: PD participants were impaired on tests from all three domains compared to control participants. Our imaging results demonstrated that successful cognition across healthy aging and Parkinson’s disease participants was related to anti-correlated coupling between the salience and default mode networks. Individuals with poorer performance scores across groups demonstrated more positive salience network/default-mode network coupling. CONCLUSIONS: Successful cognition relies on healthy coupling between the salience and default mode networks, which may become dysfunctional in PD. These results can help inform non-pharmacological interventions (repetitive transcranial magnetic stimulation) targeting these specific networks before they become vulnerable in early stages of Parkinson’s disease.Published versio

Social working memory: neurocognitive networks and directions for future research.

Navigating the social world requires the ability to maintain and manipulate information about people's beliefs, traits, and mental states. We characterize this capacity as social working memory (SWM). To date, very little research has explored this phenomenon, in part because of the assumption that general working memory systems would support working memory for social information. Various lines of research, however, suggest that social cognitive processing relies on a neurocognitive network (i.e., the "mentalizing network") that is functionally distinct from, and considered antagonistic with, the canonical working memory network. Here, we review evidence suggesting that demanding social cognition requires SWM and that both the mentalizing and canonical working memory neurocognitive networks support SWM. The neural data run counter to the common finding of parametric decreases in mentalizing regions as a function of working memory demand and suggest that the mentalizing network can support demanding cognition, when it is demanding social cognition. Implications for individual differences in social cognition and pathologies of social cognition are discussed

Altered intrinsic functional coupling between core neurocognitive networks in Parkinson\u27s disease

Parkinson3s disease (PD) is largely attributed to disruptions in the nigrostriatal dopamine system. These neurodegenerative changes may also have a more global effect on intrinsic brain organization at the cortical level. Functional brain connectivity between neurocognitive systems related to cognitive processing is critical for effective neural communication, and is disrupted across neurological disorders. Three core neurocognitive networks have been established as playing a critical role in the pathophysiology of many neurological disorders: the default-mode network (DMN), the salience network (SN), and the central executive network (CEN). In healthy adults, DMN–CEN interactions are anti-correlated while SN–CEN interactions are strongly positively correlated even at rest, when individuals are not engaging in any task. These intrinsic between-network interactions at rest are necessary for efficient suppression of the DMN and activation of the CEN during a range of cognitive tasks. To identify whether these network interactions are disrupted in individuals with PD, we used resting state functional magnetic resonance imaging (rsfMRI) to compare between-network connectivity between 24 PD participants and 20 age-matched controls (MC). In comparison to the MC, individuals with PD showed significantly less SN–CEN coupling and greater DMN–CEN coupling during rest. Disease severity, an index of striatal dysfunction, was related to reduced functional coupling between the striatum and SN. These results demonstrate that individuals with PD have a dysfunctional pattern of interaction between core neurocognitive networks compared to what is found in healthy individuals, and that interaction between the SN and the striatum is even more profoundly disrupted in those with greater disease severity

Topographic hub maps of the human structural neocortical network

Hubs within the neocortical structural network determined by graph theoretical analysis play a crucial role in brain function. We mapped neocortical hubs topographically, using a sample population of 63 young adults. Subjects were imaged with high resolution structural and diffusion weighted magnetic resonance imaging techniques. Multiple network configurations were then constructed per subject, using random parcellations to define the nodes and using fibre tractography to determine the connectivity between the nodes. The networks were analysed with graph theoretical measures. Our results give reference maps of hub distribution measured with betweenness centrality and node degree. The loci of the hubs correspond with key areas from known overlapping cognitive networks. Several hubs were asymmetrically organized across hemispheres. Furthermore, females have hubs with higher betweenness centrality and males have hubs with higher node degree. Female networks have higher small-world indices

Sleep Timing and Neurocognitive Networks in Youth

Sleep timing, particularly later midpoint of sleep, has been linked to emotion dysregulation and psychopathology. Prior adult studies link poor sleep (e.g., shorter duration, later midpoint), to altered resting-state functional connectivity (rs-FC) within and between key neurocognitive networks, particularly the default mode network (DMN), which is involved in internal thought and rumination. Importantly, many psychiatric disorders begin during adolescence, a period of shifted sleep schedules. We explored associations between midpoint of sleep and rs-FC of the DMN and other core neurocognitive networks in youth. Sleep timing was measured in 3,798 youth (11.9±0.6 years, 47.5% female) from the Adolescent Brain Cognitive Development study using Fitbit watches (over 13.1±6.5 days). Internalizing symptoms were measured using self-report and rs-FC was measured between the DMN and three neurocognitive networks: dorsal attention network (DAN), frontoparietal network (FPN), and salience network (SN). Associations between sleep timing and rs-FC were measured using linear regressions adjusting for age, sex, race, parental education, family income, puberty, and head motion. Average midpoint of sleep was 3:35 AM (range: 12:34 AM-11:27 PM). Later midpoint of sleep was associated with increased self-reported depressive symptoms. Later midpoint of sleep was associated with lower DMN-DAN rs-FC. There were no associations between midpoint of sleep and DMN-DMN, DMN-FPN, or DMN-SN network rs-FC. These results add to and extend prior studies in youth by incorporating objective measures of sleep timing (Fitbit data), and in a large national sample. Additionally, our findings may have implications for the consideration of sleep timing when designing behavioral-health interventions in youth

Perception and cognition in Parkinson's disease: a neural network perspective

Parkinson’s disease (PD) is a neurodegenerative disorder commonly presenting with perceptual and cognitive dysfunction. Whereas previous work in PD suggests that abnormal basal ganglia activity has profound effects on integrated functioning of widespread cortical networks, the relation of specific network functions to the perceptual and cognitive impairments is still poorly understood. Here, I present a series of fMRI investigations of network-level functioning in non-demented individuals with PD with the aim of elucidating these associations. Study 1 examined the neural correlates of optic flow processing in 23 individuals with PD and 17 age-matched control participants (MC). An optic flow network comprising visual motion areas V6, V3A, MT+ and visuo-vestibular areas PIVC and CSv is known to be important for parsing egomotion depth cues in humans. The hypothesis was that individuals with PD would show less activation in these regions than MC when processing optic flow. While MC participants showed robust activation in this network, PD participants showed diminished activity within MT+ and CSv. Diminished CSv activity also correlated with greater disease severity. Study 2 investigated intrinsic network organization in PD with a focus on the functional coupling among three neurocognitive networks: the default-mode network (DMN), the salience network (SN), and the central executive network (CEN). Twenty-four individuals with PD and 20 MC participants were scanned at rest. The hypothesis was that PD participants would demonstrate dysfunctional SN coupling with the DMN and CEN. Relative to MC, in PD the CEN was less positively coupled with the SN and less anti-correlated with the DMN. Study 3 investigated the association between functional coupling and cognition in the same group that participated in Study 2. As hypothesized, anti-correlated functional coupling between the SN and DMN was related to successful performance on tests of executive function, psychomotor speed, and memory retrieval in MC but not in PD, suggesting that dysfunction within these networks could underlie early cognitive deficits in PD. Together, the results from the three studies suggest that dysfunctional activity in cortical networks important for visual motion processing and neurocognitive efficiency may underlie aspects of perceptual and cognitive impairment in PD.2017-12-06T00:00:00

The organization of functional neurocognitive networks in focal epilepsy correlates with domain-specific cognitive performance

Understanding and diagnosing cognitive impairment in epilepsy remains a prominent challenge. New etiological models suggest that cognitive difficulties might not be directly linked to seizure activity, but are rather a manifestation of a broader brain pathology. Consequently, treating seizures is not sufficient to alleviate cognitive symptoms, highlighting the need for novel diagnostic tools. Here, we investigated whether the organization of three intrinsic, resting-state functional connectivity networks was correlated with domain-specific cognitive test performance. Using individualized EEG source reconstruction and graph theory, we examined the association between network small worldness and cognitive test performance in 23 patients with focal epilepsy and 17 healthy controls, who underwent a series of standardized pencil-and-paper and digital cognitive tests. We observed that the specific networks robustly correlated with test performance in distinct cognitive domains. Specifically, correlations were evident between the default mode network and memory in patients, the central-executive network and executive functioning in controls, and the salience network and social cognition in both groups. Interestingly, the correlations were evident in both groups, but in different domains, suggesting an alteration in these functional neurocognitive networks in focal epilepsy. The present findings highlight the potential clinical relevance of functional brain network dysfunction in cognitive impairment.Peer reviewe

Neuronal bases of structural coherence in contemporary dance observation

The neuronal processes underlying dance observation have been the focus of an increasing number of brain imaging studies over the past decade. However, the existing literature mainly dealt with effects of motor and visual expertise, whereas the neural and cognitive mechanisms that underlie the interpretation of dance choreographies remained unexplored. Hence, much attention has been given to the Action Observation Network (AON) whereas the role of other potentially relevant neuro-cognitive mechanisms such as mentalizing (theory of mind) or language (narrative comprehension) in dance understanding is yet to be elucidated. We report the results of an fMRI study where the structural coherence of short contemporary dance choreographies was manipulated parametrically using the same taped movement material. Our participants were all trained dancers. The whole-brain analysis argues that the interpretation of structurally coherent dance phrases involves a subpart (Superior Parietal) of the AON as well as mentalizing regions in the dorsomedial Prefrontal Cortex. An ROI analysis based on a similar study using linguistic materials (Pallier et al. 2011) suggests that structural processing in language and dance might share certain neural mechanisms

The case of late preterm birth: sliding forwards the critical window for cognitive outcome risk

Many survivors of preterm birth experience neurodevelopmental disabilities, such as cerebral palsy, visual and hearing problems. However, even in the absence of major neurological complications, premature babies show significant neuropsychological and behavioural deficits during childhood and beyond. While the clinical tools routinely used to assess neurocognitive development in those infants have been useful in detecting major clinical complications in early infancy, they have not been equally sensitive in identifying subtle cognitive impairments emerging during childhood. These methodological concerns become even more relevant when considering the case of late preterm children (born between 34 and 36 gestational weeks). Although these children have been traditionally considered as having similar risks for developmental problems as neonates born at term, a recent line of research has provided growing evidence that even late preterm children display altered structural and functional brain maturation, with potential life-long implications for neurocognitive functioning. A recent study by Heinonen put forward the hypothesis that environmental factors, in this case educational attainment, could moderate the association between late preterm birth (LPT) and neuropsychological impairments commonly associated with aging. In this paper we bring together clinical literature and recent neuroimaging evidence in order to provide two different but complementary approaches for a better understanding of the "nature-nurture" interplay underlying the lifespan neurocognitive development of preterm babies