Lecture 6-Drugs For Neurodegenerative Diseases

DRUGS USED IN DISORDERS OF THE
CENTRAL NERVOUS SYSTEM AND

TREATMENT OF PAIN
Lecture 6:
Drugs for Neurodegenerative Diseases
Marc Imhotep Cray, M.D.
CNS Pharmacology
Lecture 6
Learning Objectives:
PARKINSONISM AND ITS TREATMENT
1. The presentation of Parkinson’s disease and its underlying pathophysiology
2. The functional circuitry of the nigrostriatal system.
3. The major classes of pharmacotherapy for Parkinson’s Disease and the timeline for
their use
4. The indications, mechanism of action, adverse effects and contraindications for the
major classes of drugs used in the treatment of Parkinson’s Disease
5. The type and mechanisms of alternative treatments for Parkinson’s Disease.
PHARMACOLOGY OF STROKE AND ALZHEIMER’S DISEASE
1. The laboratory and clinical tests for ruling out reversible forms of dementia in the
elderly.
2. The drug treatments for the reversible forms of dementia.
3. The current symptomatic and theoretical preventive drug therapies for Alzheimer’s
disease.
4. The theoretical drug therapies for Huntington’s disease and ALS.
5. The preventive and symptomatic drug treatments for cerebrovascular disease.
Marc Imhotep Cray, M.D. 2

CNS Pharmacology
Classification Schema: Lecture 6
Drugs for Neurodegenerative Diseases

ANTI-PARKINSON DRUGS ANTI-ALZHEIMER DRUGS
Amantadine SYMMETREL Donepezil ARICEPT
Apomorphine APOKYN Galantamine RAZADYNE
Benztropine COGENTIN Memantine NAMENDA
Biperiden AKINETON Rivastigmine EXELON
Bromocriptine PARLODEL
Carbidopa LODOSYN ANTI-MULTIPLE SCLEROSIS DRUGS
Entacapone COMTAN Azathioprine IMURAN
Levodopa (w/Carbidopa) SINEMET Cyclophosphamide CYTOXAN
Pramipexole MIRAPEX Dexamethasone DECADRON
Procyclidine KEMADRIN Fingolimod GILENYA
Rasagiline AZILECT Glatiramer COPAXONE
Ropinirole REQUIP Dalfampridine
Rotigotine NEU PRO Interferon 1a AVONEX
Selegiline (Deprenyl) ELDEPRYL Interferon 1b BETASERON
Tolcapone TASMAR Natalizumab TYSABRI
Trihexyphenidyl ARTANE Prednisone DELTASONE
ANTI-ALS DRUGS
Riluzole RILUTEK
CNS Pharmacology
Lecture 6
CNS Neurodegenerative diseases

 Neurodegenerative diseases of CNS include:
 Parkinson’s disease
 Huntington disease
 Alzheimer’s disease
 Multiple Sclerosis (MS)
 Amyotrophic Lateral Sclerosis (ALS)
 These devastating illnesses are characterized by progressive loss of
selected neurons in discrete brain areas, resulting in characteristic
disorders of movement, cognition, or both

CNS Pharmacology
Lecture 6
Basal Nuclei (Ganglia)

COMPONENTS
 Caudate nucleus
 Putamen
 Globus pallidus
GROUPING OF THE BASAL NUCLEI (GANGLIA)
 The striatum consists of caudate nucleus and putamen
 The lentiform nucleus consists of globus pallidus and putamen
 The corpus striatum consists of lentiform nucleus and caudate
nucleus

CNS Pharmacology
Lecture 6
Striatal (Extrapyramidal) Motor System

 Striatal (Extrapyramidal) Motor System plays a role in initiation and
execution of somatic motor activity, especially willed movement
 It is also involved in automatic stereotyped postural and reflex motor
activity (e.g., normal subjects swing their arms when they walk).
 Striatal motor system includes the following structures:
1. Neocortex
2. Striatum (caudatoputamen, or neostriatum)
3. Globus pallidus
4. Subthalamic nucleus
5. Substantia nigra (i.e., pars compacta and pars reticularis)
6. Thalamus (ventral anterior, ventral lateral, and centromedian nuclei)

The basal nuclei (ganglia)
Fix JD and Brueckner JK. High yield neuroanatomy 4th ed. 2009. 7
CNS Pharmacology
Lecture 6
Motor Tracts, Basal Ganglia, and
Dopamine Pathways
 Several major neuronal tracts coordinate somatic motor functions:
 One is the pyramidal tract, whose direct motor component goes

from precentral gyrus through internal capsule and midbrain and
terminates on motor neurons in anterior horn of spinal cord (What
is another name for this tract?)
 Extrapyramidal tracts (e.g., rubrospinal, reticulospinal, and

corticoreticular) are also important for motor control

Principal fiber tracts of spinal cord:
9
CNS Pharmacology
Lecture 6
Pyramidal System
Lateral (crossed) corticospinal tract

CNS Pharmacology
Lecture 6
Motor Tracts, Basal Ganglia, and
Dopamine Pathways (2)
 The basal ganglia (including caudate nucleus, putamen, and globus
pallidus) are subcortical masses found between the cerebral cortex
and thalamus that, together with the substantia nigra, help to
coordinate movement
 A major pathway, the nigrostriatal, originates in substantia nigra and
connects with basal ganglia and other structures
o The substantia nigra receives reciprocal input from these structures plus
others
 Efferent pathways (nigrostriatal) are dopaminergic; afferent input

is from neurons containing 5-HT, GABA, and substance P
 Defects in these pathways lead to motor incoordination or incapacity

Motor Tracts, Basal Ganglia,
and Dopamine Pathways (3)
Horizontal Brain Section Showing Basal Ganglia

12
Motor Tracts, Basal Ganglia,
and Dopamine Pathways (4)
Connections of Basal Ganglia
13
CNS Pharmacology
Lecture 6
Parkinsonism: Symptoms and Defect
 Parkinsonism is a progressive neurodegenerative disease that
adversely affects motor neuron control:
 Major early symptoms are:
 tremor at rest
 bradykinesia (slowness in initiating and carrying out voluntary movements)
 muscle rigidity (cogwheel) and
 flat facial affect
 If untreated, condition worsens, leading eventually to complete
immobility and early mortality
 Prevalence is approximately 2% in persons older than 65 years
 A genetic predisposition seems likely, but environmental factors

(including viral infections and neurotoxins) may play a role
Parkinsonism: Symptoms and Defect (2)
Modified from: Lippincott Illustrated Reviews-Pharmacology Sixth Edition. 2015

 Most distinctive neuropathologic finding is progressive
loss of dopaminergic neurons of the pars compacta of
the substantia nigra
 Projections of dopaminergic neurons from substantia

nigra correlate with motor and cognitive deficits
 Degeneration of dopaminergic neurons in the

nigrostriatal tract causes loss of inhibitory dopamine
action on striatal GABAergic neurons and leads to
excessive cholinergic neuron excitation of these striatal
neurons
 Drugs such as levodopa (increases DA activity) can help
15
CNS Pharmacology
Clinical Signs of Parkinson’s Disease: Lecture 6

CNS Pharmacology
Neuropathology of Parkinson Disease: Lecture 6
 In addition to an abundance of inhibitory dopaminergic neurons, the neostriatum is also rich in

excitatory cholinergic neurons that oppose action of dopamine
 Many of symptoms of parkinsonism reflect an imbalance between excitatory cholinergic neurons

and diminished number of inhibitory dopaminergic neurons

PD Strategy of treatment
 Treatment aims to replenish dopamine, or at least
to reestablish balance between DA and ACh
influences on striatal neurons
 Dopamine cannot cross the blood-brain barrier,

so its metabolic precursor, levodopa, is used
 Most of an oral dose is rapidly converted to
dopamine by dopa decarboxylase located in
blood vessel walls (thus peripherally)
 Approximately 1% to 5% of the dose crosses
blood-brain barrier, enters metabolic
pathways of dopaminergic neurons, and is
converted to DA
18
CNS Pharmacology
Lecture 6
Levodopa:
Levodopa (L-dopa [Dopar, Larodopa]), the most effective treatment, is
metabolized by dopa decarboxylase to DA, which increases availability
of DA ( the inhibitory transmitter, in the basal ganglia)
 L-Dopa becomes effective in a few weeks, especially for reducing
rigidity and akinesia
o However, L-dopa is rapidly metabolized in peripheral tissues
(bld vessels) , so that only 1% of administered dose reaches
CNS
• Pyridoxine (vitamin B6) increases this metabolism by
activating dopa decarboxylase

CNS Pharmacology
Lecture 6
Levodopa (2)
L-Dopa should be taken on an empty stomach because large, neutral
amino acids will compete with it for absorption from gut and
transport across blood–brain barrier (BBB)
Carbidopa (Sinemet), a peripheral dopa decarboxylase inhibitor

that slows metabolism of L-dopa, is usually combined with L-dopa
 L-dopa dosage can then be reduced by 80% without changing
effectiveness
 Side effects from conversion of L-dopa to DA in periphery are
also reduced

CNS Pharmacology
Lecture 6
Levodopa (3)
 Catechol-O-methyltransferase (COMT) inhibitors prevent
methylation of L-dopa in a side pathway
o This side pathway becomes significant when dopa decarboxylase
is inhibited by carbidopa
i. Entacapone (Comtan) requires frequent dosing but is least
toxic COMT inhibitor
ii. Tolcapone (Tasmar) is longer acting but can cause
fulminating hepatic necrosis
Remember: Entacapone and tolcapone—prevent peripheral L-dopa

degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT

CNS Pharmacology
Lecture 6
Side effects from L-dopa

 Side effects from L-dopa include:
 Nausea, vomiting, and anorexia induced by stimulation of
chemoreceptor trigger zone
 severity of nausea is reduced by gradually increasing t dose into
therapeutic range and by combining L-dopa with carbidopa
 Postural hypotension
 Arrhythmias from actions of DA on the heart
 Choreiform movements due to excessive actions of DA on basal
ganglion
 Psychological disturbances that can lead to insomnia and delirium

CNS Pharmacology
Lecture 6
On–Off effects of L-Dopa Tx of PD

 On-Off effects often develop after a year or more
 These are indicative of the “wearing-off phenomena” at end of
dosage intervals and erratic effectiveness
 Patients typically have a decline in response after a few years of
therapy

CNS Pharmacology
Lecture 6
Contraindications for L-dopa:

 Contraindications for L-dopa include:
 Treatment with MAO inhibitors, because the combination can
lead to a hypertensive crisis
 Glaucoma, because L-dopa can induce mydriasis
 Psychiatric disorders (PD), especially those disorders being
treated with antipsychotic drugs, which are DA antagonists;
o However, SSRIs or mirtazapine can be tried in PD patients
who are also depressed

CNS Pharmacology
Lecture 6
DA receptor agonists: nonselective

 DA receptor agonists have effects and side effects that are similar to
L-dopa
 They are often used with L-dopa and carbidopa to reduce the ON–
OFF effects
o However, they are not active in patients who have no response
to L-dopa
i. Bromocriptine (Parlodel) and Pergolide (Permax) are
nonselective DA agonists
 Because they are ergot derivatives, they can cause
pulmonary and retroperitoneal fibrosis

CNS Pharmacology
Lecture 6
DA receptor agonists: D2 selective

ii. Pramipexole (Mirapex) and ropinirole (Requip) are selective D2-
agonists, which are very effective and have fewer side effects
Pharmacokinetics:
 Pramipexole is cleared by renal tubular secretion
o Its half life is increased by cimetidine, which interferes
with secretion of organic bases (cations)
Remember: Dopamine agonists

Ergots—bromocriptine and pergolide
Non-ergot (preferred) —pramipexole, ropinirole

CNS Pharmacology
Lecture 6
Anticholinergics:
 The anticholinergics (e.g., trihexyphenidyl [Artane]), benztropine
[Cogentin]) reduce cholinergic excitatory tone in basal ganglia
 They are most frequently used in combination with antipsychotic
drugs to reduce extrapyramidal symptoms from antipsychotic
drugs (see note box below)
 Side effects are due to central and peripheral cholinoceptor
blockade
Secondary parkinsonism: Drugs such as the phenothiazines and haloperidol,

whose major pharmacologic action is blockade of dopamine receptors in the
brain, may produce parkinsonian symptoms (also called pseudoparkinsonism).
These drugs should be used with caution in patients with Parkinson’s disease.

CNS Pharmacology
Other Drug Used to Tx PD: Lecture 6
 Amantadine (Symmetrel) is an antiviral drug (Tx influenza A and rubella) that

reduces symptoms of Parkinson’s disease
 It increases DA release, decrease DA reuptake, blocks ACh receptors, and inhibits
N-methyl-D-aspartic acid (NMDA) glutamate receptors (NMDAR)
 Tolerance to this therapeutic effect often develops within 6 months
 Adverse events ataxia, livedo reticularis
 Selegiline (Eldepryl) blocks conversion of dopamine into 3-MT by selectively inhibiting
MAO-B
 This enzyme metabolizes L-dopa, but not 5-HT or NE
 The selective decrease of DA metabolism enhances effectiveness of L-dopa with
less risk of a hypertensive crisis compared to MAO-A (Metab. 5-HT, EPI, NE)
 It can be used in combination with L-dopa, making it possible to lower the L-
dopa dosage
 Antihistamines, such as diphenhydramine (Benadryl) have some weak
therapeutic effects, which are probably due to anticholinergic actions of these
drugs
CNS Pharmacology
Lecture 6
Parkinson’s disease Tx approach:
 Order of efficacies of available drugs for PD disease is the following:
L-dopa  bromocriptine amantadine  anticholinergics
 A common approach is to use low-efficacy drugs (e.g., selegiline,

amantadine, anticholinergics) during early stages of Parkinson’s
disease and reserve L-dopa with carbidopa and dopaminergic
agonists for later stages

CNS Pharmacology
Lecture 6
Final Points on PD Tx:

 A loss of GABA or increase DA in basal ganglia can lead to the
choreiform movements that are characteristic of Huntington’s
disease
 As a result, L-dopa and anticholinergics are an inappropriate
combination
 Some reduction of symptoms can be induced by DA depleters,
antipsychotics (DA blockers), or cholinesterase inhibitors
 These treatments are largely palliative and do not cure
syndrome (choreiform movements)
Note: METHYLPHENYLTETRAHYDROPYRIDINE (MPTP)-INDUCED PARKINSONISM

MPTP is an analog of meperidine (Demerol). It destroys dopaminergic neurons in
the substantia nigra
CNS Pharmacology
Lecture 6
PD treatment strategies encapsulated:
Levodopa, Carbidopa, and Other Drugs
Class and Drug Mechanism of Action
Dopamine prodrugs Are rapidly converted to dopamine by dopa
 Levodopa decarboxylase (which is inhibited by
 Levodopa + carbidopa carbidopa)
Direct-acting dopamine agonists Bind to dopamine receptors and mimic the
 Bromocriptine, Pergolide, Pramipexole, Ropinirole action of dopamine
Indirect-acting dopamine agonist Increases dopamine release and reduces
 Amantadine dopamine reuptake into dopaminergic nerve
terminals of substantia nigra neurons (by
unknown mechanism)
MAOI Inhibits only type B isozyme
 Selegiline
Muscarinic antagonists: Have central activity (brain) as anticholinergic
 Benztropine, Biperiden, Orphenadrine, agents
Trihexyphenidyl
CNS Pharmacology
Lecture 6
PD treatment
strategies
summary
schematic
Marc Imhotep Cray, M.D. LE, T et al. First Aid for the USMLE Step 1 2015 32
CNS Pharmacology
Lecture 6
Huntington Disease and Tourette
Syndrome
 Various tremors (rhythmic oscillations around a joint), tics
(repetitive, sudden, coordinated, abnormal movements), and chorea
(irregular, unpredictable, involuntary muscle jerks) are components
of disorders of coordinated movement
 Gilles de la Tourette syndrome (which includes involuntary
verbal outbursts) is a disorder of unknown cause
 Current therapy consists primarily of haloperidol and other
dopamine D2 receptor antagonists

CNS Pharmacology
Huntington Disease and Tourette Lecture 6
Syndrome (2)
 Huntington disease is a dominantly inherited disorder
characterized by progressive chorea and dementia
 disorder is traced to a single gene defect on chromosome 4
 It is typically associated with an adult onset and a shortened
lifespan
 GABA and enzymes for ACh and GABA synthesis are deficient in
basal ganglia
 Current therapy consists usually of amine-depleting drugs, such as

tetrabenazine, or haloperidol or other dopamine D2 receptor
antagonists
 adverse drug effects: hypotension, depression, sedation,
restlessness, and parkinsonism are most common
35
CNS Pharmacology
Alzheimer Disease: Symptoms, Course, Lecture 6
and Pathology
 Alzheimer disease is a neurodegenerative disorder characterized by
progressive impairment of short-term memory and other memory,
language, and thought processes
 Functions are typically lost in reverse order in which they were attained
 In advanced stages, patients cannot perform simple activities of daily

life
 Diagnosis is usually made 3 years or more after symptom onset, and

life expectancy is approximately 7 to 10 years after diagnosis

CNS Pharmacology
Alzheimer Disease: Symptoms, Lecture 6
Course, and Pathology (2)

 Gross brain atrophy accompanies progression of
disease, with characteristic high numbers of
neuritic plaques (fragments of insoluble amyloid,
type Aβ, protein) and neurofibrillary tangles
(abnormal τ microtubule complexes), particularly in
hippocampus and posterior temporoparietal lobe
areas
 Predisposing factors include aging and genetics,
with a possible contribution from environmental
toxins
 The neurodegeneration results in loss or
dysfunction of neurotransmitter pathways

CNS Pharmacology
Alzheimer Disease: Cholinergic Lecture 6
Involvement and Drugs

 Although many NT systems become disrupted in Alzheimer disease,
cholinergic pathways become especially damaged
 Functional cholinergic deficits, such as impairment in short-term
memory, become apparent even in early stages of disease
 (SDL, Study NIP, Plates 3-21 , 3-22 and 3-23)
 Medication strategies to ameliorate the decline in cholinergic
function include the administration of precursors (eg, lecithin); direct-
acting cholinergic receptor agonists; and indirect acting
cholinomimetics
 Indirect-acting agents, specifically cholinesterase inhibitors, such
as donepezil, galantamine, and rivastigmine, are currently the
most commonly used
CNS Pharmacology
Lecture 6

CNS Pharmacology
Lecture 6
Drugs Used in Multiple Sclerosis (MS)

 MS is an autoimmune inflammatory demyelinating disease
of the CNS (effects both sensory and motor function)
 The course of MS is variable:
 For some, MS may consist of one or two acute neurologic
episodes
 In others, it is a chronic, relapsing, or progressive disease that
may span 10 to 20 years
 Historically, corticosteroids (for example, dexamethasone and
prednisone) have been used to treat acute exacerbations of the
disease
 Chemotherapeutic agents, such as cyclophosphamide and

azathioprine, have also been used
CNS Pharmacology
Lecture 6
MS Tx-Disease-modifying therapies
 Drugs currently approved for MS are indicated to decrease relapse
rates or in some cases to prevent accumulation of disability
 Major target of these medications is to modify the immune

response through inhibition of white blood cell–mediated
inflammatory processes that eventually lead to myelin sheath
damage and decreased or inappropriate axonal communication
between cells

CNS Pharmacology
Lecture 6
MS Tx-Disease-modifying therapies (2)
 Interferon β1a and interferon β1b: The immunomodulatory effects of interferon
help to diminish inflammatory responses that lead to demyelination of the axon
sheaths
 Adverse effects may include depression, local injection site rxns, hepatic
enzyme increases, and flulike symptoms
 Glatiramer: a synthetic polypeptide that resembles myelin protein and may act
as a decoy to T-cell attack
 Adverse effects some patients experience a postinjection reaction that includes
flushing, chest pain, anxiety, and itching
 It is usually self-limiting
 Fingolimod: an oral drug that alters lymphocyte migration, resulting in fewer

lymphocytes in the CNS
 Adverse effects may cause first-dose bradycardia and is associated with an
increased risk of infection and macular edema
CNS Pharmacology
Lecture 6
MS Tx-Disease-modifying therapies (3)

4. Teriflunomide: an oral pyrimidine synthesis inhibitor that leads to a lower
concentration of active lymphocytes in CNS
 Adverse effects may cause elevated liver enzymes, should be avoided in pregnancy
5. Dimethyl fumarate: an oral agent that may alter cellular response to oxidative
stress to reduce disease progression
 Adverse effects flushing and abdominal pain are most common
6. Natalizumab: a monoclonal antibody indicated for MS in patients who have failed

first-line therapies

CNS Pharmacology
Lecture 6
MS-Symptomatic treatment
 Many different classes of drugs are used to manage symptoms of MS
such as spasticity, constipation, bladder dysfunction, and depression
 Dalfampridine an oral potassium channel blocker, improves
walking speeds in patients with MS
o First drug approved for this use

CNS Pharmacology
Lecture 6
Drugs Used in Tx of Amyotrophic Lateral
Sclerosis (ALS)
 ALS is characterized by progressive degeneration of motor neurons,
resulting in inability to initiate or control muscle movement (pure
motor disease (vs MS that is motor and sensory)
 Riluzole an NMDA receptor antagonist, is currently the only drug

indicated for management of ALS
 It is believed to act by inhibiting glutamate release and blocking
sodium channels
 Riluzole may improve survival time and delay need for ventilator
support in patients suffering from ALS

CNS Pharmacology
Lecture 6
THE END

CNS Pharmacology
Further study (SDL): Lecture 6
MedPharm Digital Guidebook: Unit 3-Drugs Used for CNS Disorders
Companion eNotes: CNS- Central Nervous System Pharmacology
Textbook Reading: Aminoff MJ. Pharmacologic Management of Parkinsonism & Other
Movement Disorders In: Katzung BG, ed. Basic & Clinical Pharmacology. 12th ed. Pgs. 483-98
Online resource center: Medical Pharmacology Cloud Folder
Lectures/discussions to follow:
7. Anesthetics
8. Analgesics
9. Drugs of Abuse

Lecture 6-Drugs For Neurodegenerative Diseases

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DRUGS USED IN DISORDERS OF THE

CENTRAL NERVOUS SYSTEM AND

Marc Imhotep Cray, M.D. 2

Drugs for Neurodegenerative Diseases

CNS Neurodegenerative diseases

Marc Imhotep Cray, M.D. 4

Basal Nuclei (Ganglia)

Marc Imhotep Cray, M.D. 5

Striatal (Extrapyramidal) Motor System

Marc Imhotep Cray, M.D. 6

 One is the pyramidal tract, whose direct motor component goes

 Extrapyramidal tracts (e.g., rubrospinal, reticulospinal, and

Marc Imhotep Cray, M.D. 8

Marc Imhotep Cray, M.D. 10

 Efferent pathways (nigrostriatal) are dopaminergic; afferent input

Marc Imhotep Cray, M.D. 11

Horizontal Brain Section Showing Basal Ganglia

Connections of Basal Ganglia

 Prevalence is approximately 2% in persons older than 65 years

 A genetic predisposition seems likely, but environmental factors

Modified from: Lippincott Illustrated Reviews-Pharmacology Sixth Edition. 2015

 Projections of dopaminergic neurons from substantia

 Degeneration of dopaminergic neurons in the

Marc Imhotep Cray, M.D. 16

 In addition to an abundance of inhibitory dopaminergic neurons, the neostriatum is also rich in

 Many of symptoms of parkinsonism reflect an imbalance between excitatory cholinergic neurons

Marc Imhotep Cray, M.D. 17

 Dopamine cannot cross the blood-brain barrier,

Marc Imhotep Cray, M.D. 19

Carbidopa (Sinemet), a peripheral dopa decarboxylase inhibitor

Marc Imhotep Cray, M.D. 20

Remember: Entacapone and tolcapone—prevent peripheral L-dopa

Marc Imhotep Cray, M.D. 21

Side effects from L-dopa

Marc Imhotep Cray, M.D. 22

On–Off effects of L-Dopa Tx of PD

Marc Imhotep Cray, M.D. 23

Contraindications for L-dopa:

Marc Imhotep Cray, M.D. 24

DA receptor agonists: nonselective

Marc Imhotep Cray, M.D. 25

DA receptor agonists: D2 selective

Remember: Dopamine agonists

Marc Imhotep Cray, M.D. 26

Secondary parkinsonism: Drugs such as the phenothiazines and haloperidol,

Marc Imhotep Cray, M.D. 27

Other Drug Used to Tx PD: Lecture 6

 Amantadine (Symmetrel) is an antiviral drug (Tx influenza A and rubella) that

 A common approach is to use low-efficacy drugs (e.g., selegiline,

Marc Imhotep Cray, M.D. 29

Final Points on PD Tx:

Note: METHYLPHENYLTETRAHYDROPYRIDINE (MPTP)-INDUCED PARKINSONISM

Marc Imhotep Cray, M.D. 33

 Current therapy consists usually of amine-depleting drugs, such as

 In advanced stages, patients cannot perform simple activities of daily

 Diagnosis is usually made 3 years or more after symptom onset, and

Marc Imhotep Cray, M.D. 36

Course, and Pathology (2)

Marc Imhotep Cray, M.D. 37

Alzheimer Disease: Cholinergic Lecture 6

Involvement and Drugs

Marc Imhotep Cray, M.D. 39

Drugs Used in Multiple Sclerosis (MS)

 Chemotherapeutic agents, such as cyclophosphamide and

 Major target of these medications is to modify the immune

Marc Imhotep Cray, M.D. 41