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SEMINAR PRESENTATION
ON
NEUROPROTECTIVE NUTRIENTS
BY
AYENI OMOLARA PRECIOUS
MATRIC NUMBER: 1909001066
DEPARTMENT OF BIOCHEMISTRY
FACULTY OF SCIENCE
EKITI STATE UNIVERSITY
OUTLINE
Introduction
What are neuroprotective agents?
Clinical conditions that need neuroprotective agents
Pathophysiology of neuronal damage
Neuroprotective agents
Neuroprotective agent from natural sources: role of
phytochemicals
Conclusion
WHAT ARE NEUROPROTECTIVE NUTRIENTS?
 “Neuroprotection” is defined as a collection of processes and strategies protecting neural tissues from
cellular incidents (such as apoptosis, degeneration, and inflammation) associated with chronic
neurodegenerative diseases (e.g., Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis) as
well as those derived from acute disorders (e.g., ischemia, stroke, or trauma).
 Neuroprotective agent is medications that can alter the course of metabolic events and have
neuroprotective function.
 Neuroprotective agents are needed in patients undergoing the surgical procedure (cardiopulmonary
bypass, carotid surgery, and cerebral aneurysm surgery) and clinical
CLINICAL CONDITIONSTHAT NEED
NEUROPROTECTIVE NUTRIENTS
 Stroke: Oxidative distress, apoptotic pathway activation, and excitotoxicity subsequently emerge after cerebral ischemia,
promoting neuronal death
 Shock:A major portion of cell damage is caused by cellular ischemia
 Sepsis: Hypoperfusion and subsequent rise of serum creatinine levels, serum lactate increase, total bilirubin levels
elevation, thrombocytopenia, and acute lung injury are possible effects of severe sepsis.
 Sepsis can cause cell damage and result in neuronal damage
 Traumatic brain injury (TBI) The secondary portion of TBI will cause damage at the cellular stage with severe
consequences including the following; (1) inflammation, (2) excitotoxicity, (3) failure of nerve energy generation
PATHOPHYSIOLOGY OF NEURONAL
DAMAGE
 Free oxygen radicals
 Membrane depolarization and cerebral edema
 Tissue acidosis
 Peri-infarction depolarization
 Energy formation failure
 Mitochondrial damage
NEUROPROTECTIVE NUTRIENTS
Intravenous anesthesia agent such as; Thiopental, Propofol, Ketamine, Etomidate
 The mechanism of Intravenous anesthesia agent is exerted through incremented neuronal hypoxia tolerance,
attenuated inflammatory reactions, or decreased apoptosis-induced stress endoplasmic reticulum
COX-2 selective inhibitor
 COX-2 selective inhibitors inhibit the cyclooxygenase-2 enzyme. COX-2 converts arachidonic acid to
prostaglandins and activates NMDA receptors, stimulating inflammation. It is shown that they protect against
neurodegenerative diseases as well.
 Piracetam - include increased cholinergic neurotransmission
NEUROPROTECTIVE NUTRIENTS
Immunosuppressant agents such as; Cyclosporine A (CsA)
 One of their neuroprotective mechanisms is blocking extracellular signal-regulated kinases 1 and 2 (ERK1/2),
both bearing pro-apoptotic properties and expressed post-ischemia. FK506 inhibits calcineurin activities as well
as nitric oxide (NO) construction.
Beta-blocker
 As neuroprotective agents, beta-blockers act under a mechanism of action consisting of apoptosis inhibition,
TNF- and interleukin-1β expressions attenuation, and increased cortical microvascular perfusion
 Citicoline - increase neurotransmitters levels in the CNS
NEUROPROTECTIVE AGENT FROM NATURAL
SOURCES: ROLE OF PHYTOCHEMICALS
 The vast majority of studies on health benefits of phytochemicals have focused on the fact that many of
the active chemicals possess antioxidant activity.
 Neuroprotective effects of various phytochemicals are associated with reduced levels of oxidative stress
 Example include; Phenolic compounds, Flavonoids, Alkaloids, Terpenoids and Saponins, Fatty Acids
 Other phytochemicals of neuroprotective importance are; Hypericin and pseudohypericin, Curcumin,
Resveratrol, Allium and allicin
CONCLUSION
 Neuroprotective nutrients are used to save ischemic neurons in the brain from irreversible injury
or offer protection against cell degeneration to the neuronal cells
 Inhibiting deleterious pathways that signal to neurons (inflammation, oxidative stress, apoptosis,
and those alike) are the main molecular mechanisms of neuroprotective agents.
 Many of the phytochemicals that have recently been reported to exert neuroprotective effects
in various experimental models of neurological disorders
1909001066-1.pptx neuroprotective nutrients

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1909001066-1.pptx neuroprotective nutrients

  • 1. SEMINAR PRESENTATION ON NEUROPROTECTIVE NUTRIENTS BY AYENI OMOLARA PRECIOUS MATRIC NUMBER: 1909001066 DEPARTMENT OF BIOCHEMISTRY FACULTY OF SCIENCE EKITI STATE UNIVERSITY
  • 2. OUTLINE Introduction What are neuroprotective agents? Clinical conditions that need neuroprotective agents Pathophysiology of neuronal damage Neuroprotective agents Neuroprotective agent from natural sources: role of phytochemicals Conclusion
  • 3. WHAT ARE NEUROPROTECTIVE NUTRIENTS?  “Neuroprotection” is defined as a collection of processes and strategies protecting neural tissues from cellular incidents (such as apoptosis, degeneration, and inflammation) associated with chronic neurodegenerative diseases (e.g., Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis) as well as those derived from acute disorders (e.g., ischemia, stroke, or trauma).  Neuroprotective agent is medications that can alter the course of metabolic events and have neuroprotective function.  Neuroprotective agents are needed in patients undergoing the surgical procedure (cardiopulmonary bypass, carotid surgery, and cerebral aneurysm surgery) and clinical
  • 4.
  • 5. CLINICAL CONDITIONSTHAT NEED NEUROPROTECTIVE NUTRIENTS  Stroke: Oxidative distress, apoptotic pathway activation, and excitotoxicity subsequently emerge after cerebral ischemia, promoting neuronal death  Shock:A major portion of cell damage is caused by cellular ischemia  Sepsis: Hypoperfusion and subsequent rise of serum creatinine levels, serum lactate increase, total bilirubin levels elevation, thrombocytopenia, and acute lung injury are possible effects of severe sepsis.  Sepsis can cause cell damage and result in neuronal damage  Traumatic brain injury (TBI) The secondary portion of TBI will cause damage at the cellular stage with severe consequences including the following; (1) inflammation, (2) excitotoxicity, (3) failure of nerve energy generation
  • 6. PATHOPHYSIOLOGY OF NEURONAL DAMAGE  Free oxygen radicals  Membrane depolarization and cerebral edema  Tissue acidosis  Peri-infarction depolarization  Energy formation failure  Mitochondrial damage
  • 7. NEUROPROTECTIVE NUTRIENTS Intravenous anesthesia agent such as; Thiopental, Propofol, Ketamine, Etomidate  The mechanism of Intravenous anesthesia agent is exerted through incremented neuronal hypoxia tolerance, attenuated inflammatory reactions, or decreased apoptosis-induced stress endoplasmic reticulum COX-2 selective inhibitor  COX-2 selective inhibitors inhibit the cyclooxygenase-2 enzyme. COX-2 converts arachidonic acid to prostaglandins and activates NMDA receptors, stimulating inflammation. It is shown that they protect against neurodegenerative diseases as well.  Piracetam - include increased cholinergic neurotransmission
  • 8. NEUROPROTECTIVE NUTRIENTS Immunosuppressant agents such as; Cyclosporine A (CsA)  One of their neuroprotective mechanisms is blocking extracellular signal-regulated kinases 1 and 2 (ERK1/2), both bearing pro-apoptotic properties and expressed post-ischemia. FK506 inhibits calcineurin activities as well as nitric oxide (NO) construction. Beta-blocker  As neuroprotective agents, beta-blockers act under a mechanism of action consisting of apoptosis inhibition, TNF- and interleukin-1β expressions attenuation, and increased cortical microvascular perfusion  Citicoline - increase neurotransmitters levels in the CNS
  • 9. NEUROPROTECTIVE AGENT FROM NATURAL SOURCES: ROLE OF PHYTOCHEMICALS  The vast majority of studies on health benefits of phytochemicals have focused on the fact that many of the active chemicals possess antioxidant activity.  Neuroprotective effects of various phytochemicals are associated with reduced levels of oxidative stress  Example include; Phenolic compounds, Flavonoids, Alkaloids, Terpenoids and Saponins, Fatty Acids  Other phytochemicals of neuroprotective importance are; Hypericin and pseudohypericin, Curcumin, Resveratrol, Allium and allicin
  • 10.
  • 11. CONCLUSION  Neuroprotective nutrients are used to save ischemic neurons in the brain from irreversible injury or offer protection against cell degeneration to the neuronal cells  Inhibiting deleterious pathways that signal to neurons (inflammation, oxidative stress, apoptosis, and those alike) are the main molecular mechanisms of neuroprotective agents.  Many of the phytochemicals that have recently been reported to exert neuroprotective effects in various experimental models of neurological disorders