Neurological Disorders

Chapter 7
How do our neurons communicate
with each other?

Electrical Signal

Chemical Signal
 Do Now:

• Sleeping Beauty just pricked her finger

and is feeling a lot of pain. Model the
neurons involved in Sleeping Beauty
sensing this pain.

• In order for one neuron in this pathway

to send information to the next, how
would you change the electrical signal
of the axon into a chemical signal at
the synapse ?
 Pain Pathway

Sensory neuron

Projection neuron

Motor neuron

Interneuron
Converting an Electrical Signal to
Chemical Signal

Electrical Signal

Chemical Signal
Synaptic Transmission

Electrical Signal

Neurotransmitter
Synaptic Transmission

Electrical Signal

Neurotransmitter
 The Stage:
Presynaptic cell Synapse Postsynaptic Cell
 The Characters:
Voltage-gated
Ca2+ channels
Synaptic vesicles

Neurotransmitters (NT)
Action
Potential Ca2+ sensitive Receptors
proteins

Reuptake Transporters
 Your most common neurotransmitters
Neurotransmitter Function
Acetylcholine Gets us going. It excites cells, activates muscles, and is involved in
wakefulness, attentiveness, anger, aggression, and sexuality. Alzheimer’s
disease is associated with a shortage of acetylcholine.
Glutamate Is a major excitatory neurotransmitter. It is dispersed widely throughout the
brain. It’s involved in learning and memory.
GABA Is your brain’s main inhibitory neurotransmitter. It slows everything down
and helps keep your system in balance. It helps regulate anxiety.
Epinephrine Also known as adrenaline, keeps you alert and your blood pressure
balanced, and it jumps in when you need energy. It’s produced and released
by the adrenal glands in time of stress. Too much can increase anxiety or
tension.

Dopamine Is vital for voluntary movement, attentiveness, motivation and pleasure. It’s
a key player in addiction.
Serotonin Helps regulate body temperature, memory, emotion, sleep, appetite, and
mood. Many antidepressants work by regulating serotonin.
 NEUROLOGICAL DISORDERS

• TUMORS
• SEIZURE DISORDER
• ALZHEIMER’S DISEASE
• HUNTINGTON’S DISEASE
• DEPRESSION
 TUMOR

• A mass of cells whose growth is uncontrolled

and serves no useful function.
• Can be malignant (cancerous) or benign
(harmless) – whether the tumor is encapsuled
(border) between mass of tumor cells and
surrounding tissue.
• If surgeon removes tumor, some cells may be
missed and these cells will produce new tumor.
 TUMOR
• When cells grow old or become damaged,
they die, and new cells take their place.
Sometimes this orderly process breaks down,
and abnormal or damaged cells grow and
multiply when they shouldn't. These cells may
form tumors, which are lumps of tissue.

• Damage the brain: compression & infiltration –

Benign tumor also can give pressure to the
brain and destroy brain tissue.

• Some tumors can be destroyed by beam of

radiation focused on them.
TUMOR
 SEIZURE DISORDER

• Also known as epilepsy.

• A period of sudden,
excessive activity of
cerebral neurons.
• Can cause a convulsion
– a wild, uncontrollable
activity of the muscles.
 SEIZURE DISORDER

• Partial vs generalized & simple vs complex seizures.

• Partial seizures – a definite focus, source of irritation.
The neurons that become involved in the seizure are
restricted to a small part of the brain.
• Generalized seizures – widespread, involving most of
the brain. – grow from focus but some the origin is not
discovered.
• Simple – often cause changes in consciousness but do
not cause loss of consciousness.
• Complex – lead to loss of consciousness.
 SEIZURE DISORDER

• Grand mal – most severe form. – accompanied by

convulsion.
• Has warning symptoms – changes in mood, sudden
few jerks of muscle activity on awakening.
• Aura also happens – excitation of neurons surrounding
a seizure focus. Different for each region.
• E.g; temporal lobe – begin with feelings of dread or
occasionally euphoria.
• Tonic phase (muscles contract)  clonic phase
(jerking)
 ABSENCE SEIZURE
Absence seizures –
stop what they are
doing and stare off
into the distance for
a few seconds. Can
disrupt child’s
performance. Usually
occur on children
Alzheimer’s Disease: Burning Out with
Age?

20
 Alzheimer’s Disease: Burning Out with
Age?
• The major deficit of Alzheimer’s is the loss of
episodic memory.
• Executive functions decline throughout
Alzheimer’s disease.
• Biological markers of Alzheimer’s disease
include amyloid-beta plaques and
neurofibrillary tau tangles.

21
Alzheimer’s Disease: Burning Out with
Age?

22
Alzheimer’s Disease: Burning Out with
Age?

Beta-amyloid plaques form from Hyperphosphorylation of the

extracellular accumulations of beta- tau proteins leads them to
amyloid peptides, which are detach from microtubules
generated during the normal and clump into
metabolic activity of neurons neurofibrillary tangles. 23
 Alzheimer’s Disease: Burning Out with
Age?
• Most cases of Alzheimer’s disease occur in
individuals over age 60.
• The epsilon 4 variant of the apolipoprotein E
(ApoE4) gene seems to increase the risk of
developing the disease.
• Genetic forms of Alzheimer’s disease account
for only a small percentage of cases.

24
Alzheimer’s Disease: Burning Out with
Age?

25
 Alzheimer’s Disease: Burning Out with
Age?
• Treatment of Alzheimer’s disease
– There are currently no cures for Alzheimer’s
disease.
– No medications significantly slow down or reverse
the progression of the disease.
– Acetylcholinesterase inhibitors and NMDA
glutamate receptor antagonists sometimes slow
the progression of the disease.

26
 Alzheimer’s Disease: Burning Out with
Age?
• A potential treatment uses the immune
system to remove plaques, but this has not
resulted in any clinical improvement.
• Social, mental, and physical activity can
decrease the risk and severity of Alzheimer’s
disease.

27
Huntington’s Disease: A Genetic Rarity, in
Two Senses
• Patients perform restless involuntary
movements of the face, trunk, and limbs.
• It commonly also includes psychiatric
symptoms such as depression, apathy, anxiety,
delusions, and hallucinations.
• The biological cause is degeneration of the
anterior caudate nucleus of the striatum.

28
Huntington’s Disease: A Genetic Rarity, in
Two Senses

29
Huntington’s Disease: A Genetic Rarity, in
Two Senses

30
Huntington’s Disease: A Genetic Rarity, in
Two Senses
• Huntington’s disease is caused by the
mutation of an autosomal dominant gene.
• This mutation encodes the inclusion of a
trinucleotide repeat of the sequence CAG in
the final protein.
– Most people have fewer than 28 CAG repeats, and
this results in no issues.
– Individuals with more than 35 repeats are at an
increased risk of developing the disease.
31
Huntington’s Disease: A Genetic Rarity, in
Two Senses
• Risk factors for Huntington’s disease include
both genetic and environmental factors.
• Treatment for Huntington’s disease involves
dopamine receptor antagonists.
• These relieve some of the motor and
psychiatric symptoms.

32
Huntington’s Disease: A Genetic Rarity, in
Two Senses

33
HUNTINGTON DISEASE
 Depression: A Global Burden

• Impact of Depression
• Causes of Depression
• Neurochemical Effects of Depression on Brain
• Treatment of Depression

35
 Impact of Depression

• Depression is characterized by a low mood

that makes it difficult to carry out the
functions necessary for daily life.
• Individuals with depression do not take
pleasure in typical activities, lack motivation
and energy, and have altered sleep patterns
and appetite.

36
Impact of Depression

37
 Impact of Depression

• The worldwide incidence of depression is 5%

at any one time.
• In the United States, the incidence is 5% for
men and 10% for women.
• Lifetime incidence is roughly double the one-
time incidence rates.
• The cost of depression is estimated to be
about $80 billion per year in the U.S.

38
Impact of Depression

39
 Causes of Depression

• Mood disorders run in families, suggesting a

genetic basis.
• Depression may be an evolutionary adaptation
to suffering a trauma or defeat
• Depression causes the individual to stay away
from opponents and predators while waiting
for better times.

40
Causes of Depression

41
 Neurochemical Effects of Depression on
Brain
• Monoamine hypothesis of depression
– There is a shortage of the monoamine
neurotransmitters.
– By inhibiting the enzyme monoamine oxidase,
which breaks down these transmitters, mood will
be improved.

42
 Neurochemical Effects of Depression on
Brain
• Serotonin hypothesis
– More specific than the monoamine hypothesis.
– There is, specifically, a shortage of serotonin.
– Selective serotonin reuptake inhibitors specifically
affect serotonin levels.

43
 Neurochemical Effects of Depression on
Brain
• Other biological theories
– There are abnormalities with glutamate
neurotransmission.
– There are low levels of the neuronal growth factor
brain-derived neurotrophic factor (BDNF).

44
Neurochemical Effects of Depression on
Brain

45
 Treatment of Depression

• Three major treatments are used for

individuals with depression
– Psychotherapy
– Pharmacotherapy
– Somatic therapy

46
 Treatment of Depression

• In psychotherapy, the patient interacts with a

clinician to work through the causes of their
depression.
• Cognitive therapy is about as effective as
pharmacotherapy
• The effects seem to persist for a longer time
than the medication does.

47
Treatment of Depression

48
 Treatment of Depression

• Anti-depressant medications include

– Monoamine oxidase inhibitors (MAOIs)
– Tricyclic antidepressants (TCAs)
– Selective serotonin reuptake inhibitors (SSRIs)
• All of these are about equally effective.
• Different medications are more or less
effective for different individuals.

49
Treatment of Depression

50
 Treatment of Depression

• Somatic therapies are more invasive.

• These include
– Repetitive transcranial magnetic stimulation
– Electroconvulsive therapy
– Deep brain stimulation

51