Is Schizophrenia A Neurodevelopmental Disorder?

Schizophrenia ◽  
2019 ◽  
Author(s):  
Stephen J. Glatt ◽  
Stephen V. Faraone ◽  
Ming T. Tsuang
Keyword(s):  
Neurodevelopmental Disorder ◽  
Living Room ◽  
Normal Brain ◽  
Toxic Substances ◽  
Brain Disorder ◽  
External Agent ◽  
Brain Breaks ◽  
Disease Attack ◽  
The Brain ◽  
The Way

The research we have discussed suggests that schizophrenia occurs when ab­normal genes and environmental risk factors combine to cause brain dys­function. In the past two decades, several researchers— notably Drs Daniel Weinberger, Larry Seidman, and Patricia Goldman- Rakic— have concluded that schizophrenia is a neurodevelopmental brain disorder. This suggests that schizophrenia emerges because of the way the brain is built early in life. To understand this concept, consider brain disorders that do not have a neurodevelopmental origin but instead, come about because of the way the brain breaks down after it is developed. We call these disorders neurodegenerative be­cause the causes of the disease attack and degrade a normal brain. The senility of old age, which doctors call dementia, is a common example. When some people age, their brain is degraded by events such as many strokes or the rav­ages of Alzheimer’s disease. After a few years, a person who once functioned normally can no longer do simple tasks. Other examples are acquired brain syndromes, which occur after an injury to the head, and disorders due to the in­gestion of toxic substances (e.g., drugs, lead paint). In each of these cases, some external agent has acted on a normal brain to make it abnormal. In neurodevelopmental disorders, the brain does not develop (i.e., grow) prop­erly. In other words, it was never really normal to begin with. We know that genes contain the ‘blueprint’ for building the brain. For schizophrenia, this blueprint contains errors so that the brain is not ‘built’ correctly. Dr Patricia Goldman- Rakic suggested that certain brain cells in individuals with schizophrenia do not ‘migrate’ correctly during development. That is, normal brain development re­quires that cells locate themselves in the right spot and connect to one another in specific patterns. In schizophrenia, it may be that some cells are in the wrong place, some do not make necessary connections, and others make connections that should not be made. It is as if the blueprint for a home told the electrician to put the light switch for the kitchen in the living room.

A Life Span Developmental Approach

2005 ◽  
Author(s):  
James C. Harris
Keyword(s):  
Intellectual Disability ◽  
Brain Development ◽  
Life Span ◽  
Cognitive Processing ◽  
Network Formation ◽  
Developmental Trajectories ◽  
Neurodevelopmental Disorder ◽  
Normal Brain ◽  
The Brain ◽  
Normal Brain Development

Intellectual disability is a neurodevelopmental disorder that continues throughout the life span of the affected person. It is essential to understand how persons with intellectual disability progress throughout their life span from infancy to old age. The maturation of the brain, their environmental experiences, and the mastery of developmental challenges and tasks must all be considered. A focus on brain development is in keeping with neuroscience research indicating that progressive brain maturation is accompanied by successive synaptic reorganization as one moves from one developmental stage to the next. Anatomical Magnetic Resonance Imaging Studies are playing a major role in understanding the developmental trajectories of normal brain development (Durston et al., 2001; Giedd et al., 1999). Understanding the developmental trajectories of normal brain development is crucial to the interpretation of brain development in neurodevelopmental disabilities. During normal development, white matter volume increases with age, and although gray matter volumes increase during childhood, they decrease before adulthood. These changes in the brain are accompanied by changes in cognitive processing; for example, executive functioning shows a progressive emergence from the preschool years (Espy et al., 1999) into the adolescent years. Working memory and inhibitory processes may be measured during the preschool years. By adolescence, abstract reasoning, anticipatory planning, and mental judgment have emerged and may be measured. Cognitive abilities in adolescence are qualitatively different from those of young children as a result of the reorganization of the prefrontal cortex during maturation. How genetic background and environment interact in producing these changes is the object of ongoing study, yet investigators are beginning to understand how physiological processes of synaptic development, circuits, and neuronal network formation relate to processes of cognitive development (Fossella et al., 2003). The development of persons with intellectual disability is now being evaluated systematically, and developmental trajectories are being established for known neurogenetic syndromes. These studies are making up for a surprising lack of application of a developmental perspective to persons with intellectual disability. Developmental theorists have, for the most part, monitored and measured development in normally intelligent persons in establishing developmental landmarks.

Schizophrenia and the normal functional development of the prefrontal cortex

1990 ◽  
Vol 2 (4) ◽  
pp. 409-424 ◽  
Author(s):  
Nancy A. Breslin ◽  
Daniel R. Weinberger
Keyword(s):  
Prefrontal Cortex ◽  
Neurodevelopmental Disorder ◽  
Brain Regions ◽  
Normal Brain ◽  
Functional Development ◽  
Duration Of Illness ◽  
Normal Functional ◽  
Brain Changes ◽  
And Behavior ◽  
The Brain

AbstractSchizophrenia is being increasingly viewed as a neurodevelopmental disorder, that is, one in which early, fixed pathology becomes manifest clinically during the normal course of maturation of the brain. Evidence for this position comes first from neuroimaging research, such as (1) studies that demonstrate morphologic brain changes (such as ventriculomegaly on CT scans) even in first break patients; and (2) a lack of correlation between these morphologic changes and duration of illness. Another source of evidence is studies of normal brain development in rodents and primates, including research that shows (1) the prefrontal cortex is a late maturing part of the brain, and (2) lesions of the prefrontal cortex may be initially silent and show delayed onset of dysfunction as the brain matures. A neurodevelopmental approach to schizophrenia, in turn, has stimulated further work into the normal development of brain regions implicated in the illness, such as the frontal cortex. Thus, the fields of neuropsychiatry and neurodevelopment have been mutually stimulated during the course of this work. In addition, viewing schizophrenia in developmental terms may have implications for the understanding of changes in cognition and behavior during normal adolescence.

Metallic prions

2004 ◽  
Vol 71 ◽  
pp. 193-202 ◽  
Author(s):  
David R Brown
Keyword(s):  
Prion Protein ◽  
Binding Capacity ◽  
Normal Function ◽  
Transmissible Spongiform Encephalopathies ◽  
Published Data ◽  
Normal Brain ◽  
Copper Binding ◽  
Loss Of Function ◽  
Spongiform Encephalopathies ◽  
The Brain

Prion diseases, also referred to as transmissible spongiform encephalopathies, are characterized by the deposition of an abnormal isoform of the prion protein in the brain. However, this aggregated, fibrillar, amyloid protein, termed PrPSc, is an altered conformer of a normal brain glycoprotein, PrPc. Understanding the nature of the normal cellular isoform of the prion protein is considered essential to understanding the conversion process that generates PrPSc. To this end much work has focused on elucidation of the normal function and activity of PrPc. Substantial evidence supports the notion that PrPc is a copper-binding protein. In conversion to the abnormal isoform, this Cu-binding activity is lost. Instead, there are some suggestions that the protein might bind other metals such as Mn or Zn. PrPc functions currently under investigation include the possibility that the protein is involved in signal transduction, cell adhesion, Cu transport and resistance to oxidative stress. Of these possibilities, only a role in Cu transport and its action as an antioxidant take into consideration PrPc's Cu-binding capacity. There are also more published data supporting these two functions. There is strong evidence that during the course of prion disease, there is a loss of function of the prion protein. This manifests as a change in metal balance in the brain and other organs and substantial oxidative damage throughout the brain. Thus prions and metals have become tightly linked in the quest to understand the nature of transmissible spongiform encephalopathies.

A Survey on Detection and Classification of Brain Tumor Using Image Processing Techniques

2020 ◽  
pp. 967-973
Author(s):  
V. Deepika ◽  
T. Rajasenbagam
Keyword(s):  
Image Processing ◽  
Brain Tumor ◽  
Soft Tissues ◽  
Tumor Detection ◽  
Tumor Classification ◽  
Normal Brain ◽  
Image Processing Techniques ◽  
Normal Brain Function ◽  
Processing Techniques ◽  
The Brain

A brain tumor is an uncontrolled growth of abnormal brain tissue that can interfere with normal brain function. Although various methods have been developed for brain tumor classification, tumor detection and multiclass classification remain challenging due to the complex characteristics of the brain tumor. Brain tumor detection and classification are one of the most challenging and time-consuming tasks in the processing of medical images. MRI (Magnetic Resonance Imaging) is a visual imaging technique, which provides a information about the soft tissues of the human body, which helps identify the brain tumor. Proper diagnosis can prevent a patient's health to some extent. This paper presents a review of various detection and classification methods for brain tumor classification using image processing techniques.

8. Retrospect of Mental Philosophy (Periodical Literature.)

1880 ◽  
Vol 26 (113) ◽  
pp. 119
Author(s):  
B. F. C. Costelloe
Keyword(s):  
Periodical Literature ◽  
Main Interest ◽  
Intended Meaning ◽  
Border Line ◽  
Emotional Language ◽  
Ordinary Power ◽  
The Moment ◽  
The Brain ◽  
The Way

The first number for the year is not remarkable for any paper of striking value. Readers of the Journal will be chiefly attracted by the long and clearly written resumé of Dr. Hughlings Jackson's recent studies “On Affections of Speech from Disease of the Brain,” which is contributed by Mr. James Sully. He remarks on the great value of Dr. Jackson's attempts to classify the different forms of aphasia under the three main heads or stages of—(1) Defect of Speech, in which the patient has a full vocabulary, but confuses words; (2) Loss of Speech, in which the patient is practically speechless, and his pantomimic power is impaired as well; and (3) Loss of Language, in which, besides being speechless, he has altogether lost the power of pantomime, and even his faculty of emotional language is deeply involved in the wreck. All these states or stages again are, properly speaking, to be distinguished altogether from affections of speech in the way of loss of articulation (owing to paralysis of the tongue, &c.), or loss of vocalisation (owing to disease of the larynx); whereas the three degrees or stages of aphasia proper are due to a deep-seated and severe disorganisation of the brain. The main interest of the theory lies in the ingenious and carefully-argued analysis of the symptoms, by which Dr. Jackson arrives at the theory that as the process of destruction goes on, the superior “layers” or strata of speech fail first—those namely which involve the ordinary power of adapting sounds to the circumstances of the moment as they arise; after them fail the “more highly organized utterances” those, namely, which have in any way become automatic, such as “come on,” “wo! wo!” and even “yes” and “no,” which stand on the border-line between emotional and intellectual language; next fails the power of adapting other than vocal signs to convey an intended meaning, which is called, rather clumsily, “pantomimic propositionising;” and last of all dies out the power of uttering sounds or making signs expressive merely of emotion—a power which, of course, is not true speech at all.

scholarly journals FOXP1 syndrome: a review of the literature and practice parameters for medical assessment and monitoring

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Reymundo Lozano ◽  
Catherine Gbekie ◽  
Paige M. Siper ◽  
Shubhika Srivastava ◽  
Jeffrey M. Saland ◽  
...  
Keyword(s):  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Medical Assessment ◽  
Forkhead Box ◽  
Organ Systems ◽  
Practice Parameters ◽  
Assessment And Monitoring ◽  
Multidisciplinary Group ◽  
The Brain

AbstractFOXP1 syndrome is a neurodevelopmental disorder caused by mutations or deletions that disrupt the forkhead box protein 1 (FOXP1) gene, which encodes a transcription factor important for the early development of many organ systems, including the brain. Numerous clinical studies have elucidated the role of FOXP1 in neurodevelopment and have characterized a phenotype. FOXP1 syndrome is associated with intellectual disability, language deficits, autism spectrum disorder, hypotonia, and congenital anomalies, including mild dysmorphic features, and brain, cardiac, and urogenital abnormalities. Here, we present a review of human studies summarizing the clinical features of individuals with FOXP1 syndrome and enlist a multidisciplinary group of clinicians (pediatrics, genetics, psychiatry, neurology, cardiology, endocrinology, nephrology, and psychology) to provide recommendations for the assessment of FOXP1 syndrome.

scholarly journals The unbalanced reorganization of weaker functional connections induces the altered brain network topology in schizophrenia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rossana Mastrandrea ◽  
Fabrizio Piras ◽  
Andrea Gabrielli ◽  
Nerisa Banaj ◽  
Guido Caldarelli ◽  
...  
Keyword(s):  
Resting State ◽  
Functional Organization ◽  
Functional Integration ◽  
Brain Network ◽  
Modular Organization ◽  
Node Degree ◽  
Imaging Data ◽  
Brain Disorder ◽  
Functional Connections ◽  
The Brain

AbstractNetwork neuroscience shed some light on the functional and structural modifications occurring to the brain associated with the phenomenology of schizophrenia. In particular, resting-state functional networks have helped our understanding of the illness by highlighting the global and local alterations within the cerebral organization. We investigated the robustness of the brain functional architecture in 44 medicated schizophrenic patients and 40 healthy comparators through an advanced network analysis of resting-state functional magnetic resonance imaging data. The networks in patients showed more resistance to disconnection than in healthy controls, with an evident discrepancy between the two groups in the node degree distribution computed along a percolation process. Despite a substantial similarity of the basal functional organization between the two groups, the expected hierarchy of healthy brains' modular organization is crumbled in schizophrenia, showing a peculiar arrangement of the functional connections, characterized by several topologically equivalent backbones. Thus, the manifold nature of the functional organization’s basal scheme, together with its altered hierarchical modularity, may be crucial in the pathogenesis of schizophrenia. This result fits the disconnection hypothesis that describes schizophrenia as a brain disorder characterized by an abnormal functional integration among brain regions.

scholarly journals LSD1 enzyme inhibitor TAK-418 unlocks aberrant epigenetic machinery and improves autism symptoms in neurodevelopmental disorder models

2021 ◽  
Vol 7 (11) ◽  
pp. eaba1187
Author(s):  
Rina Baba ◽  
Satoru Matsuda ◽  
Yuuichi Arakawa ◽  
Ryuji Yamada ◽  
Noriko Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Enzyme Activity ◽  
Neurodevelopmental Disorders ◽  
Neurodevelopmental Disorder ◽  
Specific Inhibitor ◽  
Autism Spectrum ◽  
Poly I:C ◽  
Control Of Gene Expression ◽  
Epigenetic Machinery ◽  
The Brain

Persistent epigenetic dysregulation may underlie the pathophysiology of neurodevelopmental disorders, such as autism spectrum disorder (ASD). Here, we show that the inhibition of lysine-specific demethylase 1 (LSD1) enzyme activity normalizes aberrant epigenetic control of gene expression in neurodevelopmental disorders. Maternal exposure to valproate or poly I:C caused sustained dysregulation of gene expression in the brain and ASD-like social and cognitive deficits after birth in rodents. Unexpectedly, a specific inhibitor of LSD1 enzyme activity, 5-((1R,2R)-2-((cyclopropylmethyl)amino)cyclopropyl)-N-(tetrahydro-2H-pyran-4-yl)thiophene-3-carboxamide hydrochloride (TAK-418), almost completely normalized the dysregulated gene expression in the brain and ameliorated some ASD-like behaviors in these models. The genes modulated by TAK-418 were almost completely different across the models and their ages. These results suggest that LSD1 enzyme activity may stabilize the aberrant epigenetic machinery in neurodevelopmental disorders, and the inhibition of LSD1 enzyme activity may be the master key to recover gene expression homeostasis. TAK-418 may benefit patients with neurodevelopmental disorders.

The role of GABAA receptor biogenesis, structure and function in epilepsy

2006 ◽  
Vol 34 (5) ◽  
pp. 863-867 ◽  
Author(s):  
S. Mizielinska ◽  
S. Greenwood ◽  
C.N. Connolly
Keyword(s):  
Gabaa Receptor ◽  
Structure And Function ◽  
Inhibitory Synapses ◽  
Normal Brain ◽  
Synaptic Targeting ◽  
Acid Type ◽  
Normal Brain Function ◽  
And Function ◽  
The Brain

Maintaining the correct balance in neuronal activation is of paramount importance to normal brain function. Imbalances due to changes in excitation or inhibition can lead to a variety of disorders ranging from the clinically extreme (e.g. epilepsy) to the more subtle (e.g. anxiety). In the brain, the most common inhibitory synapses are regulated by GABAA (γ-aminobutyric acid type A) receptors, a role commensurate with their importance as therapeutic targets. Remarkably, we still know relatively little about GABAA receptor biogenesis. Receptors are constructed as pentameric ion channels, with α and β subunits being the minimal requirement, and the incorporation of a γ subunit being necessary for benzodiazepine modulation and synaptic targeting. Insights have been provided by the discovery of several specific assembly signals within different GABAA receptor subunits. Moreover, a number of recent studies on GABAA receptor mutations associated with epilepsy have further enhanced our understanding of GABAA receptor biogenesis, structure and function.

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