Abstract

Current models of cognition and behavioral diagnosis emphasize categorical classification over continuous considerations of function and promote the "differential diagnosis" of various conditions according to observational criteria.

However, an overemphasis on a purely behavioral, categorical approach to understanding human function fails to address the comorbidity of different disorders and does not include a consideration of overlapping levels of function, from "pathological" through "normal," to "gifted" or exceptional.

The frequent co-occurrence of "gifted" and "pathological" function is thus difficult to understand from a corticocentric and purely behavioral and observational point of view.

This article reviews "giftedness" in relation to the diagnosis of attention-deficit hyperactivity disorder, coexistence of which is termed "twice exceptional."

It additionally considers problems in assessing these functions using current neuropsychological tests and methodologies that are presumably based upon a corticocentric model of cognition.

Abstract

This article proposes a link between autistic people being misperceived by the neurotypical majority and their being at risk of poor mental health and well-being.

We present a transactional account of development in which the misperceptions (and consequent behaviour) of the neurotypical majority influences the perceptions and behaviour of autistic people such that they become increasingly separate and indeed isolated from mainstream society.

This jeopardizes their mental health and prevents autistic people from developing to full potential.

The situation is not only problematical for the development of autistic people but is also to the detriment of wider society, in so far as autistic people are effectively prevented from contributing fully.

This account assumes that some (not necessarily all) autistic people yearn to be included, to be productive and to be useful.

It thus directly opposes accounts that view autism as an extreme case of diminished social motivation.

Abstract

Prenatal infection during pregnancy increases the risk for developing neuropsychiatric disorders such as schizophrenia. This is linked to an inflammatory microglial phenotype in the offspring induced by maternal immune activation (MIA).

Microglia are crucial for brain development and maintenance of neuronal niches, however, whether and how their activation is involved in the regulation of neurodevelopment remains unclear.

Here, we used a MIA rodent model in which polyinosinic: polycytidylic acid (poly (I:C)) was injected into pregnant mice. We found fewer parvalbumin positive (PV+) cells and impaired GABAergic transmission in the dentate gyrus (DG), accompanied by schizophrenia-like behavior in the adult offspring. Minocycline, a potent inhibitor of microglia activation, successfully prevented the above-mentioned deficits in the offspring.

Furthermore, by using microglia-specific arginase 1 (Arg1) ablation as well as overexpression in DG, we identified a critical role of Arg1 in microglia activation to protect against poly (I:C) imparted neuropathology and altered behavior in offspring.

Taken together, our results highlight that Arg1-mediated alternative activation of microglia are potential therapeutic targets for psychiatric disorders induced by MIA.

Abstract

Prenatal infection during pregnancy increases the risk for developing neuropsychiatric disorders such as schizophrenia. This is linked to an inflammatory microglial phenotype in the offspring induced by maternal immune activation (MIA).

Microglia are crucial for brain development and maintenance of neuronal niches, however, whether and how their activation is involved in the regulation of neurodevelopment remains unclear.

Here, we used a MIA rodent model in which polyinosinic: polycytidylic acid (poly (I:C)) was injected into pregnant mice. We found fewer parvalbumin positive (PV+) cells and impaired GABAergic transmission in the dentate gyrus (DG), accompanied by schizophrenia-like behavior in the adult offspring. Minocycline, a potent inhibitor of microglia activation, successfully prevented the above-mentioned deficits in the offspring.

Furthermore, by using microglia-specific arginase 1 (Arg1) ablation as well as overexpression in DG, we identified a critical role of Arg1 in microglia activation to protect against poly (I:C) imparted neuropathology and altered behavior in offspring.

Taken together, our results highlight that Arg1-mediated alternative activation of microglia are potential therapeutic targets for psychiatric disorders induced by MIA.

ABSTRACT

The time is ripe to integrate burgeoning evidence of the important role of sensory and motor functioning in mental health within the National Institute of Mental Health’s [NIMH] Research Domain Criteria [RDoC] framework (National Institute of Mental Health, n.d.a), a multi-dimensional method of characterizing mental functioning in health and disease across all neurobiological levels of analysis ranging from genetic to behavioral. . . .

More than half of people diagnosed with one psychiatric disorder will be diagnosed with a second or third in their lifetime. About a third have four or more.

Our findings confirm that high comorbidity across some disorders in part reflects overlapping pathways of genetic risk,” said lead author Andrew Grotzinger, an assistant professor in the Department of Psychology and Neuroscience.

The finding could ultimately open the door to treatments that address multiple psychiatric disorders at once and help reshape the way diagnoses are given, he said.

“If you had a cold, you wouldn’t want to be diagnosed with coughing disorder, sneezing disorder and aching joints disorder,” Grotzinger said.