The researchers also unexpectedly found that the Bax gene, known for its role in apoptosis, appears to also play a role in
synaptic pruning in the dentate gyrus.
MRIs of some people with schizophrenia show that parts of their brain are smaller than normal, a feature associated with overactive
synaptic pruning in adolescence.
Further research showed that fetal mice bred to lack these molecules — like animals lacking MHCI, and like humans with autism or schizophrenia — undergo inadequate
synaptic pruning in some parts of their brains.
Not exact matches
The
synaptic connections
in motor and sensory areas are firmly established and the process of elimination synapses (
pruning)
in these areas has begun.
Maybe it did the opposite, telling neurons
in the adult brain when to let those
synaptic connections weaken — and, ultimately, be
pruned away.
Pasko Rakic at Yale University and colleagues at the University of Zagreb, Croatia, and the VU University Medical Center
in Amsterdam, the Netherlands, have now found that the brains of adults
in their 20s are still subject to
synaptic pruning.
In January 2016, a landmark study in Nature from the Broad Institute in Cambridge, Massachusetts, reported that a set of genes associated with schizophrenia can contribute to synaptic prunin
In January 2016, a landmark study
in Nature from the Broad Institute in Cambridge, Massachusetts, reported that a set of genes associated with schizophrenia can contribute to synaptic prunin
in Nature from the Broad Institute
in Cambridge, Massachusetts, reported that a set of genes associated with schizophrenia can contribute to synaptic prunin
in Cambridge, Massachusetts, reported that a set of genes associated with schizophrenia can contribute to
synaptic pruning.
In particular, widespread «
synaptic pruning» — a sort of scaling down of connectors between neurons — reshapes the brain as a child transitions to adulthood.
After conducting studies
in both humans and mice, the researchers said this new schizophrenia risk gene, called C4, appears to be involved
in eliminating the connections between neurons — a process called «
synaptic pruning,» which,
in humans, happens naturally
in the teen years.
A recent study linking schizophrenia and variations of the gene C4 also implicates the pathway involved
in synaptic pruning.
Hence, understanding how
synaptic pruning occurs may shed light on neurodevelopmental disorders and on neurodegenerative diseases
in which a
synaptic pruning gone awry may contribute to pathological synapse loss.»
What was particularly striking, Stevens notes, is that the researchers also found high expressions of C1q, a protein involved
in normal
synaptic pruning.
Specifically, converging lines of evidence suggest that mechanisms such as oxidative stress and extracellular matrix (ECM) deficit may contribute to the functional impairment of PV neurons, leading to aberrant developmental
synaptic pruning of prefrontal cortex neural circuitry and hence a failure
in the maintenance of
synaptic stability.
In addition to promoting the functional integrity of PV neurons, maturation of ECM may also play an instrumental role in the termination of developmental synaptic pruning; thus, ECM deficit can lead to excessive loss of synapses by prolonging the course of prunin
In addition to promoting the functional integrity of PV neurons, maturation of ECM may also play an instrumental role
in the termination of developmental synaptic pruning; thus, ECM deficit can lead to excessive loss of synapses by prolonging the course of prunin
in the termination of developmental
synaptic pruning; thus, ECM deficit can lead to excessive loss of synapses by prolonging the course of
pruning.
synaptic pruning The reduction
in the number of neurons and synapses that begins
in infancy and is mostly complete by early adulthood.
Synaptic pruning and other changes that occur
in the adolescent brain give teenagers the tools to start making decisions on their own — even if they're bad decisions, says Luna.
Recently, a research team led by Dr. Cynthia A. Lemere of the Ann Romney Center for Neurologic Diseases at Brigham and Women's Hospital utilized C3 - deficient mice, B6; 129S4 - C3tm1Crr / J (003641) to investigate whether the C3 - mediated
synaptic pruning mechanisms at work
in the developing brain also contribute to cognitive decline
in the aging brain.