The prefrontal cortex, which is critical for temporal organization of the cognitive processes, is among the last cortical regions to reach full functional maturity. Prefrontal functions therefore show an unusually long period of vulnerability in which neurons and glia are easily affected by internal and external insults. Furthermore, early frontal lesions can result in deficits that are not immediately apparent, but predispose to later developmental problems such as learning disabilities, attention deficit/hyperactivity disorder, and even problems with moral judgment.
To fully appreciate the implications of developmental problems in children with frontal lobe damage, hypothesis-driven studies are needed to explore functions such as working memory or executive function during childhood, instead of sole reliance on traditional intelligence tests. Two functionally and neurally distinct cognitive selection mechanisms involve the prefrontal lobes:those based on internal representations （context dependent）;and those involving exploratory processing of novel situations （context independent）. We used a cognitive bias task representing contextual reasoning to correlate lateralization with age in the frontal lobes. Young children showed context-independent responses representing right frontal lobe function, while adolescents and adults showed context-dependent responses implicating left frontal lobe function. The locus of frontal cortical control in right-handed male subjects thus shifts from right to left as cognitive contextual reasoning develops.
In daily life, we repeat decision-making from several choices consciously or unconsciously. To make decisions and perform under uncertain circumstances, deliberation about possible future consequences using probabilistic estimations of both reward and risk is required. Recently, Damasio ［Behav Brain Res, 41, 81-94, 1990］ proposed the somatic marker hypothesis （SMH） as an explanation of the processes of human decision-making. In normal controls, sympathetic skin response （SSR） always appeared 1.5～2 s after the presentation of aversive/immoral visual stimuli. However, SSR did not appear in a patient with disconnection between the orbitofrontal lobe and amygdala. Failure of a contribution of the frontal-emotional circuits to decision-making could explain patient behavior （i.e., conduction disorder）. This finding seems to be in agreement with SMH.
Our studies suggest that frontal lobe functions develop gradually, with spurts between 5 and 10 years of age, reaching completion by post-adolescence. Frontal lobe function thus shows increased vulnerability and plasticity in the second decade of life.
Human psychological mechanisms and behavioral patterns are as much the products of evolution as morphology and biochemical processes. Human technology and civilization have developed exponentially since the advent of agriculture and pastoralism. However, the basic workings of human brain were formulated during 65 million years of primate evolution, particularly during the last 200 thousand years of Homo sapiens evolution. Evolutionary psychology aims to elucidate the biological bases of human psychology utilizing knowledge about the environment in which this human evolution took place.
Recent discoveries in the fields of behavioral ecology and physical anthropology have revealed that humans are incredibly prosocial animals with deep potentials for altruism and sympathy. These characteristics are, of course, based on social abilities possessed by our closest relatives, the great apes. However, humans must have acquired this specific prosociality after diverging from the ape line, in the human-specific evolutionary environment.
Humans possess an ability for emotional empathy, in which the individual is unconsciously affected by the emotions of other individuals, as well as an ability to consciously understand and feel sympathy toward other individuals. Humans had to venture into the new environment of the savannah around 2.5 million years ago, with the gradual cooling and aridification of Africa. In order to survive this severe environment, social intelligence to understand others both cognitively and emotionally would have been crucial. However, humans have gone one step further to share the state of mind, such as “I know that you know that I know that you see the dog”. This special ability enabled us to develop language and build civilization, eventually leading to our current state on Earth.
Self-other discrimination is a basic cognitive ability for social development. Here, I introduce part of our research findings focusing on brain functions and behavioral characteristics for self-other discrimination in children with autism spectrum disorder （ASD）. First, our near-infrared spectroscopy studies have shown that, during recognition of the self-face, healthy subjects showed increased activity of the right inferior frontal gyrus （IFG） compared to the left side, while ASD children did not show this lateral dominance. Moreover, these activities in the right IFG reflected ASD severity, such that more serious ASD characteristics corresponded with lower activity levels. These findings suggest that dysfunction in the right IFG responsible for self-other discrimination is one of the crucial neural substrates underlying ASD characteristics. Second, we performed behavioral studies to investigate preferences to social stimuli that can affect the development of self-other discrimination. We used motion-tracking systems to analyze child behaviors and have found that ASD children showed lower preferences for other people than normally developing children. Based on these research findings, we hypothesized a negative spiral model for atypical development of the social brain:1） ASD children show low preference for social stimuli;2） the lower preference leads to lack of experience in ASD children performing self-other discrimination;3） ASD children might show cognitive immaturity for self-other discrimination;4） ASD children experience more and more difficulty in self-other discrimination, and lose interest in social stimuli;and 5） this loss of interest and major difficulties cause lower preferences for social stimuli. We speculate that ASD children might experience atypical development of the social brain along this spiral.
The cognitive network shows a deep relationship with the autonomic nervous system when performing cognitive tasks. We hypothesize that cognitive function may be affected by autonomic emotional responses, particularly executive function. This study was designed to clarify the involvement of the autonomic system during an executive functional task via developmental changes assessed using pupillometry. Seventeen healthy children and 9 healthy adults participated in this study. Children were divided into 3 groups （Group A, 7-9 years;Group B, 10-14 years;Group C, 15-19 years）. Pupil diameter was recorded using an eye mark recorder during the Wisconsin card sorting test （WCST）. The rate of pupil variations was integrated and compared within each age group. Categories achieved （CA） in behavioral results of WCST gradually increased with age, showing significant differences between Group A and other groups. The change rate of pupillary diameter increased with CS and decreased with consecutive correct responses and after identification of a new category in adults. The change rate of pupillary diameter with CS showed a linear increase with age, and the pattern of pupillary response at 10 to 14 years old was comparable to that in adults. The integrated rate of pupil diameter with CS increased with age, and a significant difference was seen between Group A and adults. The degree of mydriasis correlated with number of CA. These findings suggest that autonomic emotional response plays an important role as a part of the process for executive function. These findings suggest that autonomic emotional response is coupled with cognitive function.
Williams syndrome （ws） is known for its uneven cognitive abilities, especially for visuo-spatial difficulty and hyper-social tendency. Although patients abilities in expressive language are relatively strong, early language development is delayed.
In this study, early social cognition and acquisition of expressive vocabulary were longitudinally observed and yielded the following two findings.
Early social development of a young boy with WS was longitudinally investigated using modified early social communication scales （based on early social communication scales （1996 ver.） by Mundy et al. and the report by Seibert et al. （Seibert et al. Infant Mental Health J3, 244-58）） and development of joint attention before uttering words was especially delayed. The numbers of expressive vocabularies measured by MacArthur communicative development inventory （word and gesture version） increased with the ability for joint attention. This may suggest that, as in typical children, joint attention plays an important role in children with WS in acquiring vocabulary in Japanese.
Vocabulary in each area of seven WS children at the language level of 36 months was compared to that of typically developing children using the MacArthur communicative development inventory （word and grammar version）. Spatial vocabulary （“locations and places”） is smaller in WS in Japanese, as in European languages, probably due to the visuo-spatial difficulty, as previously described. In addition, the smaller vocabulary compared to the TD in the area of “words about Time” may also be related to the relative dysfunction of the parietal lobe. These findings need to be evaluated further.
Human cognitive functions such as memory declined dueto the effects of aging. However, little is known about the neural mechanisms underlying age-related changes in social cognition. Recent functional magnetic resonance imaging （fMRI） studies have demonstrated that interacting mechanisms between brain regions related to social cognition and memory-related regions contribute to memory processes in social contexts. In addition, there is fMRI evidence that the effects of social context on memory processes are found in both young and older adults, but the effects involve different neural systems. These findings could reflect compensatory mechanisms supporting social cognition in the elderly. Investigations of age-dependent changes of memory in a social context could help us to understand the neural mechanisms underlying social cognition in older adults.
The clinical judgement criteria of “Kouji-Noukinou-Shyougai” including social behavioral dysfunction, were published in 2004 in Japan. Social behavioral dysfunction should be diagnosed due to social brain damage and thus be treated under cognitive rehabilitation. The medial prefrontal cortex （MPFC）, orbital PFC, temporal lobe including amygdala, and complex regions mentioned above are considered as lesions responsible for social behavioral dysfunction. Methods of cognitive rehabilitation, such as Comprehensive-Holistic Neuropsychological Rehabilitation, should be commenced as early as possible after brain injury and continued during demanding periods.
The Diagnostic and Statistical Manual of Mental Disorders, fifth edition, proposed 6 domains of cognitive function:complex attention, executive function, learning and memory, language, perceptual-motor and social cognition. Social cognition is the ability “to understand others and yourself”, including theory of mind （ToM） and self-insights.
A recent meta-analysis showed a decline in ToM in Alzheimer’s disease （AD） as well as in frontotemporal dementia （FTD）, but whether ToM deficits are independent of cognitive functioning, or the deficits are related to those of executive and/or memory functioning is controversial. ToM deficits could lead to poor social integration, social difficulties and social miscommunication. The pragmatic language disorder and decline of non-verbal communication functioning could also be related to social miscommunication in AD. We have reported declines in communicative competence for metaphor and sarcasm （irony） understanding in AD. We also reported declines in comprehension for facial expression. We compared the sensitivity of 6 basic facial expressions （happiness, sadness, surprise, fear, disgust, and anger） among the mild AD group, aged normal controls, and young normal controls. The AD group was less sensitive than aged normal controls in recognition of 5 expressions other than happiness. Within the AD group, happiness offered significantly higher sensitivity than the other five expressions. Such positivity bias needs to be confirmed in further studies.
Regarding self-insights, anosognosia, a deficit of insight into disease, has been discussed in FTD and AD. With disease progression, patients with FTD and AD tend to overestimate their own functions and abilities. Anosognosia in MCI is controversial and the functioning of self-insights could be highly individual. It is suggested that patients who retain insights tend to be depressive and anxious, whereas insight deficits may be associated with more severe caregiver burden.
Perspective-taking is a common factor in ToM and self-insights;ToM is the ability to evaluate others from a third-person perspective, whereas self-insight is the ability to evaluate the self from a third-person perspective. Studies to delineate the relationship between those two functions therefore represent important research for social cognition in dementia.
The deficits of social cognition in dementia can lead to poor social integration, and support for better social participation is desired. For better support, evaluation of social cognition is informative to understanding the social difficulties of each individual with dementia.
Several topics on apraxia of speech（AOS）are discussed. Although many lines of evidence indicate that the responsible region for AOS is the precentral gyrus, AOS-like symptoms are observable in cases with subcortical lesions such as putaminal hemorrhage or infarction in the corona radiata. Differentiating between AOS and other types of dysarthria may be difficult by error vaviability, which has traditionally been considered an important characteristic of AOS. AOS may be described as an articulation disorder that is not explicable by basic sensory motor deficits. AOS is an important, but not the only factor, contributing to non-fluent speech.
I have presented several key points to diagnose dementia with Lewy bodies （DLB） in the early stage. DLB shows relatively preserved memory, but disproportional impairment of visuospatial and executive functions compared to Alzheimer’s disease （AD）. Including tests such as drawing figures and trail-making tests may be helpful in screening for DLB. Impaired imitation of finger configurations are more frequent in DLB than in other dementias such as AD, so that finding also supports a diagnosis of DLB. Compared to early AD, early DLB frequently shows several characteristic symptoms, including REM sleep behavior disorder （RBD）, day-time somnolence, fluctuation, easy falls, visual hallucinations, illusions, misidentifications, anxiety, depression, hyposmia, and constipation. In particular, RBD and depression can precede other clinical symptoms of DLB by several years. DLB shows more errors than AD in the pareidolia test, and this may be useful for early diagnosis of DLB. Although each symptom may be nonspecific for DLB, combinations of these early symptoms offer clues to suspicion of early DLB. Detections of these early signs and symptoms, with use of essential neuroimaging, will facilitate early diagnosis of DLB.
The criterion-based validity of the Japanese version of the Mini Mental State Examination（MMSE-J） （Sugishita 2006） was preliminarily evaluated in 2010（Sugishita, Hemmi and JADNI 2010） based on data from 313 subjects who participated in the Japanese Alzheimer’s Disease Neuroimaging Initiative （J-ADNI）. Test-retest reliability was also preliminarily examined in 145 subjects in J-ADNI who were tested twice. The second testing was performed 6 months after the first（Sugishita, Hemmi and JADNI 2010）. However, in March, 2012, an employee of a pharmaceutical company reported that the J-ADNI data for some subjects had been falsified. In March, 2014, Drs. Sugishita, M and Asada,T reported a total of 105 cases with confirmed or suspected falsification of data or protocol violation （68 cases by Sugishita and 37 cases by Asad） to the Special Investigative Committee of the University of Tokyo. In June 20, 2014, the Committee confirmed that data had been inappropriately modified by inappropriate persons.
The authors （Sugishita & Hemmi） of the 2010 paper （Sugishita, Hemmi and JADNI 2010）then proposed to withdraw and revise the paper. The editorial board of the Japanese Journal of Cognitive Neuroscience accepted the proposal on June 3, 2014. In October 2014, 129 cases with confirmed or suspected falsification of data or protocol violation were reported to the Third Party Panel of the University of Tokyo. The Third Party Panel examined all 129 subjects and found no falsification of data or protocol violations. However, the four written refutations by Dr. M. Sugishita argued against the criticism of the Third Party Panel and it became clear that the Third Party Panel had made errors in judgment （cf. http://www.geocities.jp/shinjitunodentatu/daisannsyaiin.html）. Consequently, it is necessary to exclude the subjects with falsification of data or protocol violation from the J-ADNI data. However, Dr. T. Iwatsubo （the J-ADNI principal investigator） disclosed under limitations the uncorrected J-ADNI data to researchers through the Japan Science and Technology Information Aggregator, Electronic （J-STAGE） in January 2016 （http://humandbs.biosciencedbc.jp/hum0043-v1）. Therefore, the aim of the present study was to reexamine the validity and reliability of the MMSE-J after excluding cases with confirmed or suspected falsification of data or protocol violations.
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