Porcelli et al. (2019). Social brain, social dysfunction and social withdrawal.
Neuroscience Biobehavioral Reviews 97, 10 - 33.
highlights of the paper
1. the human brain shows levels of specialization for social stimuli processing
2. social brain could be affected by several psychiatric disorders
3. mechanisms underlying social dysfunction are largely similar across disorders
4. social dysfunction and social withdrawal may represent a transdiagnostic domain.
read the paper as a framework of hypotheses and try to understand and remember the core
message: “all knowledge is provisional, temporary, capable of refutation at any moment”
core message
- complex social environments were a selective pressure for the human brain
- the high complexity is associated with a high susceptibility to social psychopathology
abstract
- social deficits can be the first signs of in “non-social” psychiatric disorders
schizophrenia (SCZ), Alzheimer’s disease (AD) and major depressive disorder
(MDD) and lead to a progressive social dysfunction
- (social deficits of course are the fundamental to SAD, ASPD, AUtism, BD)
- social dysfunction and social withdrawal seen in AD, SCZ, and MDD suggest that in
these disorders the social brain is affected in similar ways
core message in one sentence
- the article aims to provide a view of the neurobiological substrates of social
functioning and to show how in three frequent and disabling neuropsychiatric
disorders (i.e. AD, SCZ and MDD) similar maladaptive mechanisms underlie social
withdrawal, which may represent an innovative transdiagnostic domain, for targeted
interventions
strenghts
- linking social deficits to psychiatric disorders not commonly regarded as social
disorders, the focus on social withdrawal, the neural networks presented in figure 1
and figure 2 and implicated neural models
- the brain models/ hypotheses of the paper are strong, based upon, and can be tested
in humans, and align with the workgroups of the course
weakness
- the neurotransmitter story is mostly and selectively based upon rodent research, is
not falsifiable (in humans), and neglects steroid hormones and most of human
research
exam
- the neurotransmitter parts of the Borcelli et paper are informative nonetheless
- read the material but not study for your exam or workgroups
Neuroscience Biobehavioral Reviews 97, 10 - 33.
highlights of the paper
1. the human brain shows levels of specialization for social stimuli processing
2. social brain could be affected by several psychiatric disorders
3. mechanisms underlying social dysfunction are largely similar across disorders
4. social dysfunction and social withdrawal may represent a transdiagnostic domain.
read the paper as a framework of hypotheses and try to understand and remember the core
message: “all knowledge is provisional, temporary, capable of refutation at any moment”
core message
- complex social environments were a selective pressure for the human brain
- the high complexity is associated with a high susceptibility to social psychopathology
abstract
- social deficits can be the first signs of in “non-social” psychiatric disorders
schizophrenia (SCZ), Alzheimer’s disease (AD) and major depressive disorder
(MDD) and lead to a progressive social dysfunction
- (social deficits of course are the fundamental to SAD, ASPD, AUtism, BD)
- social dysfunction and social withdrawal seen in AD, SCZ, and MDD suggest that in
these disorders the social brain is affected in similar ways
core message in one sentence
- the article aims to provide a view of the neurobiological substrates of social
functioning and to show how in three frequent and disabling neuropsychiatric
disorders (i.e. AD, SCZ and MDD) similar maladaptive mechanisms underlie social
withdrawal, which may represent an innovative transdiagnostic domain, for targeted
interventions
strenghts
- linking social deficits to psychiatric disorders not commonly regarded as social
disorders, the focus on social withdrawal, the neural networks presented in figure 1
and figure 2 and implicated neural models
- the brain models/ hypotheses of the paper are strong, based upon, and can be tested
in humans, and align with the workgroups of the course
weakness
- the neurotransmitter story is mostly and selectively based upon rodent research, is
not falsifiable (in humans), and neglects steroid hormones and most of human
research
exam
- the neurotransmitter parts of the Borcelli et paper are informative nonetheless
- read the material but not study for your exam or workgroups
