48 research outputs found
Childrenâs Internal Attributions of Anxiety-Related Physical Symptoms: Age-Related Patterns and the Role of Cognitive Development and Anxiety Sensitivity
The present study examined age-related patterns in childrenâs anxiety-related interpretations and internal attributions of physical symptoms. A large sample of 388 children aged between 4 and 13Â years completed a vignette paradigm during which they had to explain the emotional response of the main character who experienced anxiety-related physical symptoms in a variety of daily situations. In addition, children completed measures of cognitive development and anxiety sensitivity. Results demonstrated that age, cognitive development, and anxiety sensitivity were all positively related to childrenâs ability to perceive physical symptoms as a signal of anxiety and making internal attributions. Further, while a substantial proportion of the younger children (i.e., <7Â years) were able to make a valid anxiety-related interpretation of a physical symptom, very few were capable of making an internal attribution, which means that children of this age lack the developmental prerequisites for applying physical symptoms-based theories of childhood anxiety
Cortical dynamics and subcortical signatures of motor-language coupling in Parkinsonâs disease
ABSTRACT: Impairments of action language have been documented in early stage Parkinsonâs disease (EPD). The action-sentence compatibility effect (ACE) paradigm has revealed that EPD involves deficits to integrate action-verb processing and ongoing motor actions. Recent studies suggest that an abolished ACE in EPD reflects a cortico-subcortical disruption, and recent neurocognitive models highlight the role of the basal ganglia (BG) in motor-language coupling. Building on such breakthroughs, we report the first exploration of convergent cortical and subcortical signatures of ACE in EPD patients and matched controls. Specifically, we combined cortical recordings of the motor potential, functional connectivity measures, and structural analysis of the BG through voxelbased morphometry. Relative to controls, EPD patients exhibited an impaired ACE, a reduced motor potential, and aberrant frontotemporal connectivity. Furthermore, motor potential abnormalities during the ACE task were predicted by overall BG volume and atrophy. These results corroborate that motor-language coupling is mainly subserved by a cortico-subcortical network including the BG as a key hub. They also evince that action-verb processing may constitute a neurocognitive marker of
EPD. Our findings suggest that research on the relationship between language and motor domains is crucial to develop models of motor cognition as well as diagnostic and intervention strategies
Noninvasive optical inhibition with a red-shifted microbial rhodopsin
Optogenetic inhibition of the electrical activity of neurons enables the causal assessment of their contributions to brain functions. Red light penetrates deeper into tissue than other visible wavelengths. We present a red-shifted cruxhalorhodopsin, Jaws, derived from Haloarcula (Halobacterium) salinarum (strain Shark) and engineered to result in red lightâinduced photocurrents three times those of earlier silencers. Jaws exhibits robust inhibition of sensory-evoked neural activity in the cortex and results in strong light responses when used in retinas of retinitis pigmentosa model mice. We also demonstrate that Jaws can noninvasively mediate transcranial optical inhibition of neurons deep in the brains of awake mice. The noninvasive optogenetic inhibition opened up by Jaws enables a variety of important neuroscience experiments and offers a powerful general-use chloride pump for basic and applied neuroscience.McGovern Institute for Brain Research at MIT (Razin Fellowship)United States. Defense Advanced Research Projects Agency. Living Foundries Program (HR0011-12-C-0068)Harvard-MIT Joint Research Grants Program in Basic NeuroscienceHuman Frontier Science Program (Strasbourg, France)Institution of Engineering and Technology (A. F. Harvey Prize)McGovern Institute for Brain Research at MIT. Neurotechnology (MINT) ProgramNew York Stem Cell Foundation (Robertson Investigator Award)National Institutes of Health (U.S.) (New Innovator Award 1DP2OD002002)National Institute of General Medical Sciences (U.S.) (EUREKA Award 1R01NS075421)National Institutes of Health (U.S.) (Grant 1R01DA029639)National Institutes of Health (U.S.) (Grant 1RC1MH088182)National Institutes of Health (U.S.) (Grant 1R01NS067199)National Science Foundation (U.S.) (Career Award CBET 1053233)National Science Foundation (U.S.) (Grant EFRI0835878)National Science Foundation (U.S.) (Grant DMS0848804)Society for Neuroscience (Research Award for Innovation in Neuroscience)Wallace H. Coulter FoundationNational Institutes of Health (U.S.) (RO1 MH091220-01)Whitehall FoundationEsther A. & Joseph Klingenstein Fund, Inc.JPB FoundationPIIF FundingNational Institute of Mental Health (U.S.) (R01-MH102441-01)National Institutes of Health (U.S.) (DP2-OD-017366-01)Massachusetts Institute of Technology. Simons Center for the Social Brai
Spin Symmetry Requirements in Density Functional Theory: The Proper Way to Predict Magnetic Coupling Constants in Molecules and Solids
Environmental and anthropogenic factors affecting the probability of occurrence of Oncomegas wageneri (Cestoda: Trypanorhyncha) in the southern Gulf of Mexico
EFFECT OF MUTANT HUNTINGTIN ON STRIATAL NEURONS DIFFERENTIATED FROM HUNTINGTONâS DISEASE INDUCED PLURIPOTENT STEM CELLS
Huntingtonâs disease (HD) is an autosomal dominant disorder
caused by expansion of polyglutamine (CAG) repeats in the Huntingtin gene, leading to loss of striatal and cortical neurons
and deficits in coordinated movements and cognition. Transgenic
rodent models are valuable for testing cell death mechanisms
and therapeutic intervention. However, mouse and rat
models may not fully represent the human condition. Induced
pluripotent stem (iPS) cells, which show striking similarities to
embryonic stem cells, can now be derived from human adult
somatic tissues and have the capacity to be lineage restricted
into various neuronal subtypes. More importantly, recent studies
have been successful in generating patient specific iPS cells
from a variety of diseases including amyotrophic lateral sclerosis,
spinal muscular atrophy, Parkinsonâs disease, and HD.
Using lentiviral mediated over-expression of Oct4, Sox2,
Nanog, Lin28, cMyc and Klf4, we successfully generated iPS
cell lines from three fibroblast samples: (1) from a 6 year old
affected male with 180 CAG repeats, (2) from a 29 year old
affected female with 60 CAG repeats, and (3) from a 21 year
old unaffected female with 33 CAG repeats. We have generated
striatal neurons from these three lines in order to determine the
affect CAG repeat length has on neuronal health and survival.
In order to accelerate these studies a consortium of researchers
has been formed who are currently assessing the phenotype of
neurons generated from these iPS lines. Studies are ongoing
amongst the consortium members in order to establish a CAGdependent
HD phenotype in these lines