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Neuroplasticity in adults
Domina Petric, MD
Synaptogenesis
Synaptogenesis is creation of new
synapses.
Synaptogenesis is most active in the
early postnatal life up to 3 years.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Brain size in autism spectrum disorder
There is an increased synaptogensis in early postnatal life
with brain overgrowth.
There is increase in size of frontal and temporal cortex,
amygdala and cerebellum in comparisson to the normal
brain.
The overgrowth of the brain tends to normalize with the
time, but aberrant connections remain during the adult life.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Brain size in ADHD
There is decrease in rate of
synaptogenesis.
Frontal and temporal cortex is thinner
than in children without ADHD.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Gray matter volume
There is a reduction in gray matter volume
during the childhood and adolescence: loss of
synaptic connections.
Loss of synaptic connections is accelerated in
individuals with ADHD.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
White matter volume
There is an increase in white matter
volume during childhood and
adolescence: increase of myelination,
increase of axons diameter and/or
increase in number of axons.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Overall brain size
▪ There is increase in brain size during first decade of life and in second
decade of life there is a plato of the brain size.
▪ In the third decade of life there is a gradual decline in brain size: gray
matter is declining, whilst white matter is expanding.
▪ In the fourth decade of life there is a reduction in both gray matter and
white matter of brain.
▪ Decrase in brain size is due to reduction of myelin (white matter) and
reduction of synapses (gray matter).
▪ Loss of neurons is pathological and it is not attributable to normal brain
aging.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Peripheral nerve injury and regeneration
▪ Injured axon has a significant regenerative capacity.
▪ When there is injury to an axon, there will be degeneration of distal parts
from the injured site.
▪ Macrophages invade the injured region and consume debris.
▪ Schwann cells then will proliferate and will create a chanel through wich
the regenerating axon will hit his proximal target.
▪ Schwann cells are key mediators of regeneration and regrowth of injured
axon.
▪ They release axon growth-promoting signals and neurotrophins that will
activate expression of growth-related genes in neuron body.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Peripheral nerve injury and regeneration
There is never a full
functional recovery of
injured peripheral nerve.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Excitotoxicity
Excitotoxicity is destruction of neurons
due to release of GLUTAMATE.
This can happen during acute injury to
the nervous system.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Apoptosis stimuli
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Apoptosis
▪ Apoptosis stimuli interupt the normal function of Bcl-2 signal.
▪ When Bcl-2 is blocked, cytochrome C is released by mitochondria
leading to the activation of CASPASE-9 and CASPASE-3.
Apoptosis is then activated:
▪ chromosome condensation
▪ DNA fragmentation
▪ membrane blebbing
▪ cytoskeletal changes
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Penumbra
▪ Penumbra relates to the neurons just peripheral to the injured site in CNS.
▪ These neurons will survive.
▪ Glial cells proliferate in the site of injury and release chemical signals that have
negative effect on the growth and regeneration of survived neurons.
▪ Microglia phagocites the debris.
▪ Oligodendrocytes then proliferate.
▪ Glial cells will form a scar of tissue.
▪ Regeneration of axons that run through the white matter of the brain is difficult
because of negative glial cells effect on growth and regeneration.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Penumbra
Neurons that have axons in gray matter
(horizontal axons) will regenerate
because they are not that much
exposed to suppressive signals of the
neuroglia: adaptive plasticity after
injury.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Adult neurogenesis
Production of new neurons in adult human brain is
limited to a special set of stem cells in the basal
region of the dentate gyrus of the hippocampus.
This is important for learning and creation of new
memories.
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
Literature
https://www.coursera.org/learn/medical-
neuroscience: Leonard E. White, PhD,
Duke University
HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY

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Neuroplasticity in adults

  • 2. Synaptogenesis Synaptogenesis is creation of new synapses. Synaptogenesis is most active in the early postnatal life up to 3 years. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 3. Brain size in autism spectrum disorder There is an increased synaptogensis in early postnatal life with brain overgrowth. There is increase in size of frontal and temporal cortex, amygdala and cerebellum in comparisson to the normal brain. The overgrowth of the brain tends to normalize with the time, but aberrant connections remain during the adult life. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 4. Brain size in ADHD There is decrease in rate of synaptogenesis. Frontal and temporal cortex is thinner than in children without ADHD. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 5. Gray matter volume There is a reduction in gray matter volume during the childhood and adolescence: loss of synaptic connections. Loss of synaptic connections is accelerated in individuals with ADHD. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 6. White matter volume There is an increase in white matter volume during childhood and adolescence: increase of myelination, increase of axons diameter and/or increase in number of axons. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 7. Overall brain size ▪ There is increase in brain size during first decade of life and in second decade of life there is a plato of the brain size. ▪ In the third decade of life there is a gradual decline in brain size: gray matter is declining, whilst white matter is expanding. ▪ In the fourth decade of life there is a reduction in both gray matter and white matter of brain. ▪ Decrase in brain size is due to reduction of myelin (white matter) and reduction of synapses (gray matter). ▪ Loss of neurons is pathological and it is not attributable to normal brain aging. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 8. Peripheral nerve injury and regeneration ▪ Injured axon has a significant regenerative capacity. ▪ When there is injury to an axon, there will be degeneration of distal parts from the injured site. ▪ Macrophages invade the injured region and consume debris. ▪ Schwann cells then will proliferate and will create a chanel through wich the regenerating axon will hit his proximal target. ▪ Schwann cells are key mediators of regeneration and regrowth of injured axon. ▪ They release axon growth-promoting signals and neurotrophins that will activate expression of growth-related genes in neuron body. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 9. Peripheral nerve injury and regeneration There is never a full functional recovery of injured peripheral nerve. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 10. Excitotoxicity Excitotoxicity is destruction of neurons due to release of GLUTAMATE. This can happen during acute injury to the nervous system. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 12. Apoptosis ▪ Apoptosis stimuli interupt the normal function of Bcl-2 signal. ▪ When Bcl-2 is blocked, cytochrome C is released by mitochondria leading to the activation of CASPASE-9 and CASPASE-3. Apoptosis is then activated: ▪ chromosome condensation ▪ DNA fragmentation ▪ membrane blebbing ▪ cytoskeletal changes HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 13. Penumbra ▪ Penumbra relates to the neurons just peripheral to the injured site in CNS. ▪ These neurons will survive. ▪ Glial cells proliferate in the site of injury and release chemical signals that have negative effect on the growth and regeneration of survived neurons. ▪ Microglia phagocites the debris. ▪ Oligodendrocytes then proliferate. ▪ Glial cells will form a scar of tissue. ▪ Regeneration of axons that run through the white matter of the brain is difficult because of negative glial cells effect on growth and regeneration. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 14. Penumbra Neurons that have axons in gray matter (horizontal axons) will regenerate because they are not that much exposed to suppressive signals of the neuroglia: adaptive plasticity after injury. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 15. Adult neurogenesis Production of new neurons in adult human brain is limited to a special set of stem cells in the basal region of the dentate gyrus of the hippocampus. This is important for learning and creation of new memories. HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY
  • 16. Literature https://www.coursera.org/learn/medical- neuroscience: Leonard E. White, PhD, Duke University HTTPS://WWW.COURSERA.ORG/LEARN/MEDICAL-NEUROSCIENCE: LEONARD E. WHITE, PHD, DUKE UNIVERSITY