scholarly journals Brain Syndemics: Cognitive Deficit, Pathways of Interaction, and the Biology of Inequality

2021 ◽  
pp. 1-12
Author(s):  
Merrill Singer ◽  
Merrill Singer

Children born into and raised in disadvantaged families tend to experience poorer health and more developmental delays, lower achievement, and a greater number of behavioural and emotional problems than children from wealthier homes. There is growing evidence that poverty and social inequality leave their imprint on brain structure as well. The brain exhibits considerable plasticity, one expression of which is shaped by the biology of inequality. A specific consequence is cognitive deficit found among children raised in poverty and subject to social discrimination. This paper argues that several pathways impacted by poverty, including chronic stress, malnutrition, exposure to heightened levels of air pollution, and other toxin exposures, syndemically link social inequality to underlying neural mechanisms and to suboptimal brain development and structure. These deficits need not be permanent and are reversible through urgently needed structural, socio-economic intervention.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Florian Bitsch ◽  
Philipp Berger ◽  
Andreas Fink ◽  
Arne Nagels ◽  
Benjamin Straube ◽  
...  

AbstractThe ability to generate humor gives rise to positive emotions and thus facilitate the successful resolution of adversity. Although there is consensus that inhibitory processes might be related to broaden the way of thinking, the neural underpinnings of these mechanisms are largely unknown. Here, we use functional Magnetic Resonance Imaging, a humorous alternative uses task and a stroop task, to investigate the brain mechanisms underlying the emergence of humorous ideas in 24 subjects. Neuroimaging results indicate that greater cognitive control abilities are associated with increased activation in the amygdala, the hippocampus and the superior and medial frontal gyrus during the generation of humorous ideas. Examining the neural mechanisms more closely shows that the hypoactivation of frontal brain regions is associated with an hyperactivation in the amygdala and vice versa. This antagonistic connectivity is concurrently linked with an increased number of humorous ideas and enhanced amygdala responses during the task. Our data therefore suggests that a neural antagonism previously related to the emergence and regulation of negative affective responses, is linked with the generation of emotionally positive ideas and may represent an important neural pathway supporting mental health.


1989 ◽  
Vol 155 (S7) ◽  
pp. 93-98 ◽  
Author(s):  
Nancy C. Andreasen

When Kraepelin originally defined and described dementia praecox, he assumed that it was due to some type of neural mechanism. He hypothesised that abnormalities could occur in a variety of brain regions, including the prefrontal, auditory, and language regions of the cortex. Many members of his department, including Alzheimer and Nissl, were actively involved in the search for the neuropathological lesions that would characterise schizophrenia. Although Kraepelin did not use the term ‘negative symptoms', he describes them comprehensively and states explicitly that he believes the symptoms of schizophrenia can be explained in terms of brain dysfunction:“If it should be confirmed that the disease attacks by preference the frontal areas of the brain, the central convolutions and central lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by the disease. On various grounds, it is easy to believe that the frontal cortex, which is specially well developed in man, stands in closer relation to his higher intellectual abilities, and these are the faculties which in our patients invariably suffer profound loss in contrast to memory and acquired ability.” Kraepelin (1919, p. 219)


1995 ◽  
Vol 7 (3) ◽  
pp. 396-407 ◽  
Author(s):  
Argye E. Hillis ◽  
Alfonso Caramazza

We report the performance of a patient who, as a consequence of left frontal and temporoparietal strokes, makes far more errors on nouns than on verbs in spoken output tasks, but makes far more errors on verbs than on nouns in written input tasks. This double dissociation within a single patient with respect to grammatical category provides evidence for the hypothesis that phonological and orthographic representations of nouns and verbs are processed by independent neural mechanisms. Furthermore, the opposite dissociation in the verbal output modality, an advantage for nouns over verbs in spoken tasks, by a different patient using the same stimuli has also been reported (Caramazza & Hillis, 1991). This double dissociation across patients on the same task indicates that results cannot be ascribed to "greater difficulty" with one type of stimulus, and provides further evidence for the view that grammatical category information is an important organizational principle of lexical knowledge in the brain.


2009 ◽  
Vol 364 (1522) ◽  
pp. 1407-1416 ◽  
Author(s):  
Katherine Woollett ◽  
Hugo J. Spiers ◽  
Eleanor A. Maguire

While there is widespread interest in and admiration of individuals with exceptional talents, surprisingly little is known about the cognitive and neural mechanisms underpinning talent, and indeed how talent relates to expertise. Because many talents are first identified and nurtured in childhood, it can be difficult to determine whether talent is innate, can be acquired through extensive practice or can only be acquired in the presence of the developing brain. We sought to address some of these issues by studying healthy adults who acquired expertise in adulthood. We focused on the domain of memory and used licensed London taxi drivers as a model system. Taxi drivers have to learn the layout of 25 000 streets in London and the locations of thousands of places of interest, and pass stringent examinations in order to obtain an operating licence. Using neuropsychological assessment and structural and functional magnetic resonance imaging, we addressed a range of key questions: in the context of a fully developed brain and an average IQ, can people acquire expertise to an exceptional level; what are the neural signatures, both structural and functional, associated with the use of expertise; does expertise change the brain compared with unskilled control participants; does it confer any cognitive advantages, and similarly, does it come at a cost to other functions? By studying retired taxi drivers, we also consider what happens to their brains and behaviour when experts stop using their skill. Finally, we discuss how the expertise of taxi drivers might relate to the issue of talent and innate abilities. We suggest that exploring talent and expertise in this manner could have implications for education, rehabilitation of patients with cognitive impairments, understanding individual differences and possibly conditions such as autism where exceptional abilities can be a feature.


1998 ◽  
Vol 10 (1) ◽  
pp. 1-34 ◽  
Author(s):  
Alfonso Caramazza ◽  
Jennifer R. Shelton

We claim that the animate and inanimate conceptual categories represent evolutionarily adapted domain-specific knowledge systems that are subserved by distinct neural mechanisms, thereby allowing for their selective impairment in conditions of brain damage. On this view, (some of) the category-specific deficits that have recently been reported in the cognitive neuropsychological literature—for example, the selective damage or sparing of knowledge about animals—are truly categorical effects. Here, we articulate and defend this thesis against the dominant, reductionist theory of category-specific deficits, which holds that the categorical nature of the deficits is the result of selective damage to noncategorically organized visual or functional semantic subsystems. On the latter view, the sensory/functional dimension provides the fundamental organizing principle of the semantic system. Since, according to the latter theory, sensory and functional properties are differentially important in determining the meaning of the members of different semantic categories, selective damage to the visual or the functional semantic subsystem will result in a category-like deficit. A review of the literature and the results of a new case of category-specific deficit will show that the domain-specific knowledge framework provides a better account of category-specific deficits than the sensory/functional dichotomy theory.


2018 ◽  
Vol 115 (43) ◽  
pp. E10187-E10196 ◽  
Author(s):  
Michael A. van der Kooij ◽  
Tanja Jene ◽  
Giulia Treccani ◽  
Isabelle Miederer ◽  
Annika Hasch ◽  
...  

Stringent glucose demands render the brain susceptible to disturbances in the supply of this main source of energy, and chronic stress may constitute such a disruption. However, whether stress-associated cognitive impairments may arise from disturbed glucose regulation remains unclear. Here we show that chronic social defeat (CSD) stress in adult male mice induces hyperglycemia and directly affects spatial memory performance. Stressed mice developed hyperglycemia and impaired glucose metabolism peripherally as well as in the brain (demonstrated by PET and induced metabolic bioluminescence imaging), which was accompanied by hippocampus-related spatial memory impairments. Importantly, the cognitive and metabolic phenotype pertained to a subset of stressed mice and could be linked to early hyperglycemia 2 days post-CSD. Based on this criterion, ∼40% of the stressed mice had a high-glucose (glucose >150 mg/dL), stress-susceptible phenotype. The relevance of this biomarker emerges from the effects of the glucose-lowering sodium glucose cotransporter 2 inhibitor empagliflozin, because upon dietary treatment, mice identified as having high glucose demonstrated restored spatial memory and normalized glucose metabolism. Conversely, reducing glucose levels by empagliflozin in mice that did not display stress-induced hyperglycemia (resilient mice) impaired their default-intact spatial memory performance. We conclude that hyperglycemia developing early after chronic stress threatens long-term glucose homeostasis and causes spatial memory dysfunction. Our findings may explain the comorbidity between stress-related and metabolic disorders, such as depression and diabetes, and suggest that cognitive impairments in both types of disorders could originate from excessive cerebral glucose accumulation.


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