Neuroprotective drugs aim to protect neurons from damage in conditions like stroke. Currently, there are no approved neuroprotective treatments for stroke. Various targets of neuroprotection have been investigated including inflammation, oxidative stress, excitotoxicity, and apoptosis. Many agents have shown promise in animal models but failed in clinical trials. Edaravone is the only drug approved in Japan for acute ischemic stroke. Ongoing research continues to explore new targets and combinations of therapies to develop effective neuroprotective treatments for stroke.
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
Vymada Tablet (ARNI: Angiotensin Receptor Neprilysin Inhibitor) is an anti-hypertensive drug used in combination with Sacubitril & Valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction.
SGLT2 inhibitors in Heart failure: A prized addition to HF treatment optionsahvc0858
Early Diabetes and Dyslipidaemia Treatment Optimisation.
Presentation by Dr Chan Wan Xian
Cardiologist, Echocardiologist
Heart Failure Intensivist
Asian Heart & Vascular Centre
www.ahvc.com.sg
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
Vymada Tablet (ARNI: Angiotensin Receptor Neprilysin Inhibitor) is an anti-hypertensive drug used in combination with Sacubitril & Valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction.
SGLT2 inhibitors in Heart failure: A prized addition to HF treatment optionsahvc0858
Early Diabetes and Dyslipidaemia Treatment Optimisation.
Presentation by Dr Chan Wan Xian
Cardiologist, Echocardiologist
Heart Failure Intensivist
Asian Heart & Vascular Centre
www.ahvc.com.sg
Medicinal Cannabis in the Treatment of Parkinson'sJames Van Geelen
An overview of the MMJ program in CT, cannabis' benefits in the treatment of parkinson's disease and an introduction to the world of medicinal cannabis.
NEURODEGENERATION & NEUROPROTECTION-AN AYURVEDIC PERSPECTIVE.
WHAT AYURVEDA CAN OFFER BOTH IN PREVENTION & TREATMENT.FAMOUS PEOPLE SUFFERING FROM NEURODEGENERATION.MANDUKPARNI,SHANKHAPUSPI,POMGRENATE,ASWAGANDHA.BUDDHIBHRANSHA.NILANJAN DATTA.ROGNIDAN.PARKINSON,MULTIPLE SCLEROSIS,HUNTINGTONS CHOREA,ALZHEIMERS IN AYURVEDA TREATMENT.THANK YOU.ACKNOWLEDGEMENTS.DR.B.C.JANA.BHU.IPGAER AT SVSP,KOLKATA.BHU.
Astrocytes in the Synapse: Nurse or Key-Player?Rune Rasmussen
Astrocytes have for decades been considered as non-excitable support cells of the central nervous system (CNS). However, this view has changed radically during the last thirty years. Astrocytes have come to the forefront of neuroscience in our attempt to gain a better understanding of the cellular mechanisms underlying synaptic transmission. Astrocytes express a variety of surface receptors for common neurotransmitters, e.g., glutamate and acetylcholine. Additionally, astrocytes respond to stimulation by releasing gliotransmitters such as glutamate. These properties have led to the concept of tripartite synapse involving bidirectional communication between neurons and astrocytes. This review aims at summarizing current evidence for how astrocytes are involved in modulating synaptic transmission within cortical regions of the CNS. The activation of metabotropic- and ionotropic receptors expressed in astrocytes triggers an increase in their intracellular Ca2+ concentration, which in turn promotes the release of glutamate. The astrocyte released glutamate stimulate either group I or II and III metabotropic glutamate receptors (mGluRs) on presynaptic terminals. Depending on the type of activated presynaptic mGluR, astrocytic glutamate may either potentiate or depress synaptic transmission. In summary, astrocytes are actively participating in the modulation of synaptic transmission within cortical regions of the CNS. Astrocytes may consequently be a potential therapeutic target for brain pathological illnesses, e.g., neurodegeneration during ischemic stroke.
Christopher McKay - Rensselaer Polytechnic Institute - Doctoral Defense Prese...Christopher McKay
Christopher McKay - Rensselaer Polytechnic Institute - Doctoral Thesis Defense
Title: Hydrogels for Acute Spinal Cord Injury: Physical/Chemical Material Characterization and Assessment of Astrocytic Response
The dance between Glia and Neurons is critical to the development and maintenance to CNS. Did you know: • up to 90% of the cells in the vertebrate nervous system are “not neurons” • make > 50% of the brain volume. This is a great overview to anyone that wants to learn more.
Neuroprotection is a fairly misunderstood term in glaucoma. The ppt aims at making the reader understand the basics of neuroprotection and also the various agents available to aid it.
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxNeurologyKota
emergence of autoimmune neuropathies and role of nodal and paranodal regions in their pathophysiology.
Peripheral neuropathies are traditionally categorized into demyelinating or axonal.
dysfunction at nodal/paranodal region key for better understanding of patients with immune mediated neuropathies.
antibodies targeting node and paranode of myelinated nerves have been increasingly detected in patients with immune mediated neuropathies.
have clinical phenotype similar common inflammatory neuropathies like Guillain Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy
they respond poorly to conventional first line immunotherapies like IVIG
This presentation briefs out the approach of dementia assessment in line with consideration of recent advances. Now the pattern of assessment has evolved towards examining each individual domain rather than lobar assessment.
This presentation contains information about Dementia in Young onset. Also it describes the etiologies, clinical feature of common YOD & their management.
Entrapment Syndromes of Lower Limb.pptxNeurologyKota
This presentation contains information about the various Entrapment syndromes of Lower limb in descending order of topography. It also contains information about etiology, clinical features and management of each of these entrapment syndromes with special emphasis on electrodiagnostic confirmation.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
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Stay informed, stay safe, and get your flu shot today!
2. • Neuroprotection is specifically defined as the “protection of
neurons” and is a strategy used to potentially protect the brain in
a number of different cerebral conditions including Parkinson’s
disease, traumatic brain injury and ischemic stroke.
3. • There are currently no approved treatments for the myriad of
damaging pathological processes that persist in the brain long
after the acute stage.
• Include processes of inflammation, excitotoxicity, oxidative
stress, apoptosis, and edema resulting from disruption of the
blood brain barrier.
• In hemorrhagic stroke, additional processes include physical
damage from mass of accumulated blood itself, cytotoxicity of
blood components, and vasospasm in subarachnoid hemorrhage
4. Pathogenesis and pathophysiology of ischemic
stroke
• Deprivation of oxygen supply to the brain tissue leads to
activation of the ischemic cascade with a series of molecular
mechanisms.
• There is depletion of adenosine triphosphate and consequent
high levels of lactate and unbuffered hydrogen ions.
• These hydrogen ions facilitate the generation of ferrous iron-
mediated free radicals that result in astroglial injury.
5. • Failure of energy dependent mechanisms including ion pumps
leads to deterioration of membrane ion gradients, opening of
selective and unselective ion channels, and equilibration of most
intracellular and extracellular ions .
• Thus potassium ions leave the cell, sodium, chlorine and
calcium enter and many excitatory neurotransmitters
(glutamate, aspartate) are released in potentially toxic
concentrations.
6. • Raised intracellular calcium accelerates many potentially
injurious processes.
• Calcium activates phospholipases which hydrolyse membrane-
bound glycerophospholipids to free fatty acids and these in turn
facilitate free radical peroxidation of other membrane bound
lipids.
• Calcium similarly activates both proteases that lyse structural
proteins as well as nitric oxide synthase that initiates free radical
mechanism.
7. • Intracellular entry of calcium is made largely possible by the
activation of two types of receptors: Voltage gated (L-type)
and/or several N-methyl-D-aspartate (NMDA) and quisqualate
(Q) post synaptic receptor/channel complexes by glutamate.
8.
9. MECHANISMS OFACTION
1. Prevention of Early Ischemic Injury
2. Prevention of Reperfusion Injury
1. Prevention of Early Ischemic Injury
• Neuroprotective agents limits acute injury to neurons in
ischemic penumbra.
• Neurons in the penumbra are less likely to suffer irreversible
injury at early time points than are neurons in the infarct core.
• Many of these agents modulate neuronal receptors to reduce
release of excitatory neurotransmitters, which contribute to
early neuronal injury.
10. 2. Prevention of Reperfusion Injury
• Neuroprotective agents prevent potentially detrimental events
associated with return of blood flow.
• Although return of blood flow to the brain is generally
associated with improved outcome, reperfusion may contribute
to additional brain injury.
• Returning blood contains leukocytes that may occlude small
vessels and release toxic products.
• Neuroprotective agents that work primarily during reperfusion
may have a longer window of therapeutic effect than drugs that
work earlier in the ischemic cascade.
11. Targets for Neuroprotection in Stroke
a. Inflammation.
b. Oxidative Stress.
c. Blood-Brain Barrier Disruption.
d. Excitotoxicity.
e. Apoptosis.
f. Autophagy
12.
13. • Many different neuroprotection approaches targeting different
aspects of the ischemic cascade were tested previously in
animal stroke models and clinical development programs.
• Despite many successful treatment experiments in animals
regarding both infarct size reduction and improved functional
outcome, no neuroprotective drug demonstrated unequivocal
efficacy in clinical trials.
14.
15.
16. NEUROPROTECTIVEAGENTS FOR TREATMENTOF
STROKE
Prevention of Early Ischemic Injury
1. Free Radical Scavengers
a. Edaravone
Exerts antioxidant effects by inhibiting hydroxyl radical-
dependent and -independent lipid peroxidation
Also suppresses the increase in the levels of hydroxyl and
superoxide anion radicals
Unlike other free radical scavengers, edaravone readily crosses
the blood–brain barrier (BBB)
17. Japanese Guidelines for the management of stroke 2009 suggest
edaravone for the treatment of acute ischemic stroke as a grade B
recommendation.
Currently only approved in Japan.
Administration of edaravone within 72 h of ischemic stroke onset
significantly reduces infarct volume and provides sustained
benefits over a 3-month follow-up period
Recent study showed that administration of edaravone during tPA
infusion could enhance recanalization in 40 patients with acute
ischemic stroke
18. Tirilazad Did not show benefit in an acute stroke trial.
Drug also was investigated in subarachnoid hemorrhage
and in traumatic brain injury
NXY-059 Phase 3 trials Stroke-Acute Ischemic NXY Treatment
(SAINT I), SAINT II
SUN N4057 or
Piclozotan,
Serotonin agonist
TS-011 Blocks the synthesis of 20-hydroxyeicosatetraenoic acid
(20-HETE)
Lovastatin,
Normobaric oxygen.
Ebselen
19. 2. Modulatingthe N-methyl-D-aspartate receptors
Dextromethorphan Noncompetitive NMDA antagonist and metabolite of
cough suppressant,
Caused hallucinations and agitation; it also produced
hypotension.
GV150526 Safe and well tolerated,
No improvement was observed in any of the 3-month
outcome measures.
Magnesium Reduce ischemic injury by increasing regional blood
flow, antagonizing voltage-sensitive calcium channels,
and blocking NMDA receptor,
Intravenous Magnesium Efficacy Study (within 12 hours)
Administration of Stroke Therapy—Magnesium Phase III
(FAST-MAG) Trial.
20. NA-1 Reduces NMDA mediated injury by disrupting down-
stream pathways, associated with a reduction in MRI-based
infarcts
Selfotel,
Aptiganel HCl
(Cerestat)
Competitive NMDA antagonist
Trials were stopped prematurely
21. • 3. Modulating non NMDA receptors
Nalmefene
(Cervene)
Narcotic receptor antagonist that reduces levels of excitatory
neurotransmitters
No clinical benefit was found in a phase III trial
Lubeluzole Block sodium channels, reduce the release of nitric oxide, a
neurotransmitter generated by activation of the NMDA
receptor. Not effective
Clomethiazole g-aminobutyric acid agonist, decreases excitatory
neurotransmission
Clomethiazole Acute Stroke Study.- result was negative
Calcium channel
blockers
Nimodipine is of value in preventing secondary ischemic
infarction as a result of vasospasm following subarachnoid
haemorrhage.
a-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid
antagonist, ONO 2506,
Serotonin agonist repinotan,
22. Piracetam Positive allosteric modulator of the AMPA receptor,
Act on ion channels or ion carriers, thus leading to increased
neuron excitability,
Increase cell membrane permeability.
Exert its global effect on brain neurotransmission via modulation
of ion channes.
Cochrane review of 1002 pts
No difference between the treatment and control groups for
functional outcome, dependence or proportion of patients dead
or dependent. Adverse effects were not reported.
23. • Others
High-dose human albumin
Apart from functioning as a haemodiluent, albumin induces
systemic mobilization of n-3 polyunsaturated fatty acids and help
to replenish polyunsaturated fatty acids lost from neural
membranes.
Trial, however, was stopped early for futility.
24. Hypothermia
• Reduces brain damage from ischemia by preventing disruption
of the brain-blood barrier.
• It also lowers the basal metabolic rate and counteracts the
ischemic cascade in the penumbra.
• One study is evaluating hypothermia (treatment within 300 min)
in conjunction with a combination of caffeine and ethanol.
• Cooling in Acute Stroke (COAST-II) trial,
• Controlled Hypothermia in Large Infarction (CHILI) trial
• European Stroke Research Network for Hypothermia
(EuroHYP)-1 trial
25. Prevention of Reperfusion Injury
4. Anti-adhesion antibodies
anti-ICAM-
1 (Enlimomab)
Block an intercellular adhesion molecule (ICAM) on
the endothelium to prevent adhesion of white blood
cells to the vessel wall.
Treated subjects were found to have higher mortality
rates and worse outcomes than subjects in the placebo
group.
Human antileukocytic
antibody, Hu23F2G
Phase III trial showed no benefits.
Tetracycline antibiotics Shown to reduce leukocyte infiltration.
Phase I dose-finding trial using minocycline to treat
ischemic stroke (6-h window) was completed.
In addition to providing potential neuroprotection,
minocycline also appears to decrease levels of matrix
metalloproteinase-9, which has been associated with
recombinant tissue plasminogen activator (rtPA)–
associated cerebral hemorrhage.
26. • 5. Membrane stabilization
Citicoline
• Precursor of phosphatidylcholine, vital component of neuronal
membrane.
• Reduces the dysfunction of BBB, decreases cerebral edema,
activates cerebral energy metabolism.
• Provides the cytidine & choline. Choline is essential for the
synthesis of Acetylcholine (the cholinergic neurotransmitter)
• Inhibits Phospholipase A2 thereby :
• preserves neuronal membrane integrity
• promotes neuronal membrane repair
• inhibits the release of free fatty acids & ARA
• inhibits free radical damage
27. • A phase II trial showed improved outcome in stroke patients
treated with either a 500- or 2000-mg/d dose of citicoline.
• A post hoc subgroup analysis of the phase III trial suggested
that patients with more severe strokes (National Institutes of
Health Stroke Scale >8) had better functional outcome with
citicoline.
• A large international trial, ICTUS Study: International
Citicoline Trial on acUte Stroke enrolled 2298 patients with
moderate-to-severe strokes within 24 hours of stroke onset.
Trial did not show efficacy for citicoline compared with
placebo.
28. 6. Neuronal healing
Trafermin Basic fibroblast growth factor, help regulate neuronal
healing after ischemia.
Epoetin Beta Have anti-apoptotic and anti-inflammatory effects, to
mobilize endothelial progenitor cells into the circulation,
and to enhance angiogenesis.
Yip et al.- significantly reduced the occurrence of major
adverse neurological events (defined as recurrent stroke,
NIHSS ≥ 8, or death) after treatment for 90 days after
acute ischemic stroke
Filgrastim Granulocyte colony stimulating factor (G-CSF) reduced
infarct size, prevented BBB damage, and had an anti-
inflammatory effect
AX200 for the treatment of ischemic stroke (AXIS)-2
29.
30. Neuroprotection in Hemorrhagic Stroke
• Pathologies of ischemic and hemorrhagic stroke share many of
the same damaging processes, such as inflammation, oxidative
stress, and excitotoxicity.
• Treatments that are neuroprotective in one may also be
beneficial in the other,
• Processes such as cytotoxicity, however, are unique to
hemorrhagic stroke and are directly related to the accumulation
of blood in the brain.
31. Heme oxygenase
(HO) Inhibitor
Inhibit Heme oxygenase (HO) that converts heme to
iron and other products.
Free iron reacts with hydrogen peroxide to form
hydroxyl radicals, leading to oxidative stress.
Deferoxamine Chelation of iron
Free iron reacts with hydrogen peroxide to form
hydroxyl radicals, leading to oxidative stress.
Valproic acid Decreases the expression of HO-1
32. NEUROPROTECTANT FOR PREVENTION OFSTROKE
• Antihypertensive Drugs
Valsartan Reduces cerebral NADPH oxidase activity and levels of reactive
oxygen species, Prevents neuronal apoptosis, suppression of
inflammatory cytokines such as monocyte chemoattractant
protein1 (MCP1) and tumor necrosis factor (TNF)-α
Japanese Investigation of Kinetic Evaluation in Hypertensive
Event and Remodeling Treatment (JIKEI HEART) study
Kyoto Heart study
New or recurrent stroke was significantly reduced, by 40%, in
the valsartan group
Losartan,
Eprosartan and
Telmisartan
Losartan Intervention For Endpoint reduction in hypertension
(LIFE) study compared losartan and the β-blocker atenolol
Morbidity and Mortality After Stroke, Eprosartan Compared
with Nitrendipine for Secondary Prevention (MOSES) study
Ongoing Telmisartan Alone and in Combination with Ramipril
Global Endpoint Trial (ONTARGET) study , PRoFESS
33. • Lipid-Lowering Drugs
Atorvastatin Lowered lipid levels; decreased collagen-induced platelet
aggregation; improved whole blood viscosity; improved red
blood cell deformability; improved von Willebrand factor
activity; and improved endothelial dysfunction
decreased markers of oxidative stress and inflammatory
angiogenesis
Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT)
study
Collaborative Atorvastatin Diabetes Study (CARDS)
Participants had no documented previous history of
cardiovascular disease, an LDL-cholesterol concentration of
4.14 mmol/L or lower, a fasting triglyceride level of 6.78
mmol/L or less, and at least one of the following:
retinopathy, albuminuria, current smoking or hypertension.
The incidence of stroke was significantly reduced by 48%
with atorvastatin.
34. Simvastatin Scandinavian Simvastatin Survival Study (4S), 4444 patients
with angina pectoris or previous MI and serum cholesterol 5.5–
8.0 mmol/L on a lipid-lowering diet were randomized to
double-blind treatment with simvastatin or placebo . Over the
5.4 years median follow-up period, simvastatin significantly
lowered the incidence of stroke, by 30%.
Pravastatin CARE study
Rosuvastatin JUPITER study, 17,802 apparently healthy men and women
were randomly assigned to rosuvastatin or placebo. Patients
with normal lipid levels but elevated high-sensitivity C-
reactive protein showed a 48% reduction in the risk of stroke
when taking rosuvastatin, a reduction that was significant.
35. • Hypoglycemic Drugs
Pioglitazone Inhibits oxidative stress , it increases adiponectin levels in
patients with metabolic syndrome and it improves
endothelial dysfunction in cerebral vessels in patients with
T2DM
Recurrent stroke was significantly reduced by 47% in
patients with a prior history of stroke who received
pioglitazone compared with those treated with placebo in
the Prospective Pioglitazone Clinical Trial in
Macrovascular Events (PROACTIVE) study
40. REFERRENCES
• Neuroprotective Agents in Stroke Overview of Neuroprotective Agents
Dec 2015
• Neuroprotection for Stroke: Current Status and Future Perspectives Int. J.
Mol. Sci. 2014, 13, 11753-11772; doi:10.3390/ijms130911753
• Neuroprotection in Stroke: Past, Present, and Future ISRN Neurology
Volume 2014, Article ID 515716
• New Approaches to Neuroprotective Drug Development AHA Stroke.
2011;42[suppl 1]:S24-S27.)
• Ischemic Stroke and Neuroprotection Ann Med Health Sci Res. 2014 Jul-
Dec; 2(2): 186–190.
• Clinical Neuroprotective Drugs for Treatment and Prevention of Stroke
Int. J. Mol. Sci. 2012, 13, 7739-7761; doi:10.3390/ijms13067739
• Clinical trial registry
• Uptodate.com