Schizophrenia as a disorder of developmentally reduced synaptic connectivity.

By Thomas H. McGlashan, Ralph Hoffman. Archives of General Psychiatry, 2000

655 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/b318cd6608174a5ff35be14ebeb6272dcbb8aa0b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cognitive Neuroscience

1. Stephen M. Smith
2. E. T. Rolls
3. Gustavo Deco
4. Timothy Edward John Behrens
5. Heidi Johansen-Berg
6. Olaf Sporns
7. Mark Jenkinson
8. Gwenaëlle Douaud

In Radiology, Nuclear Medicine and Imaging

1. Stephen M. Smith
2. Heidi Johansen-Berg
3. Timothy Edward John Behrens
4. Gwenaëlle Douaud
5. Mark Jenkinson
6. Paul M. Matthews
7. Olaf Sporns
8. Christian F. Beckmann

Citations in the corpus

• Disrupted-in-Schizophrenia-1 (DISC1) regulates spines of the glutamate synapse via Rac1 (2010, background): “Deficits in postnatal synaptic pruning at glutamate synapses that occur just before the onset have been hypothesized as a potential mechanis”
• The developing brain and neural plasticity: Implications for normality, psychopathology, and resilience. (2015, background): “Thus, it appears likely that the processes underlying the normal development and maturation of cortical circuitry and connectivity may have gone awry in Schizophrenia (Arnold, 1999; Benes, 1995; McGlashan & Hoffman, 2000; Weinberger, 1987).”
• The hippocampus in schizophrenia: a review of the neuropathological evidence and its pathophysiological implications (2004, background): “This “molecular synaptic pathology” would be essentially congruent with the concept of “aberrant synaptic plasticity”, as has been advocated to occur in schizophrenia (Stevens 1992; Keshavan et al. 1993; Port and Seybold 1995; McGlashan and Hoffman 2000).”
• Prediction of psychosis in youth at high clinical risk: a multisite longitudinal study in North America. (2008, methodology): “The use of prediction algorithms with 80% PPP will enable more selective recruitment into prevention programs (minimizing exposure of false-positive cases to potential adverse events) and facilitate studies attempting to elucidate neural and other changes proximal to the onset of psychosis.(22,63,64”
• The Contribution of Early Traumatic Events to Schizophrenia in Some Patients: A Traumagenic Neurodevelopmental Model (2001, background): “Having reviewed studies finding an association be-dysfunction to genetics and perinatal events (McGlashan and Hoffman 2000). tween cortisol release and severity of schizophrenic symptoms, they highlight researchIn “Schizophrenia: A Neural DiathesisStress Model,” Walker and DiForio (1997)…”
• Computational models of schizophrenia and dopamine modulation in the prefrontal cortex (2008, background): “Hoffman and colleagues have further shown that pruning simulations of speech-perception networks that were trained with the artificial 'backpropagation of error' algorithm can result in spontaneous output (that is, output without input), and this was related to positive symptoms of schizophrenia, su”
• Anatomically related grey and white matter abnormalities in adolescent-onset schizophrenia. (2007, background): “Functional consequences of loss of white matter integrity Inter- and intra-hemispheric connectivity disturbances have been suggested to play a major role in schizophrenia (McGlashan and Hoffman, 2000; Stephan et al., 2006).”
• A developmental psychopathology perspective on adolescence. (2002, background): “…changes that take place during late adolescence and early adulthood, such as (a) synaptic pruning of the prefrontal cortex (Feinberg, 1982; McGlashan & Hoffman, 2000), (b) pubertal increases in gonadal hormones during adolescence (Spear, 2000a, 2000b), (c) developmental transformations in…”
• S100B in brain damage and neurodegeneration (2003, background): “Changes in brain structure and volume appear to arise from reduction of neuritic processes (such as dendrites and synapses) rather than from a loss of neuronal or glial cell bodies (for review see McGlashan and Hoffman, 2000).”
• Human studies of prepulse inhibition of startle: normal subjects, patient groups, and pharmacological studies (2001, background): “This integrated, multi-site activity or neural circuit is thought to be impaired in schizophrenia and other psychiatric disorders (Swerdlow and Koob 1987; Andreasen 1999; McGlashan and Hoffman 2000 ).”