Chemical Control of Brain,
Brain Disorders (Parkinson's
& Alzheimer's Disease)
Emotion
Md.Mostafizur Rahman
Faculty Of Engineering and Technology
Islamic University, Bangladesh
Department of Biomedical Engineering
Chemical Control of Brain (Neurotransmitters)
Introduction
★ Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a
target cell across a synapse
★Synapses are the junctions where neurons release a chemical neurotransmitter that acts
on a postsynaptic target cell, which can be another neuron or a muscle or gland cell
★Some chemicals released by neurons have little or no direct effects on their own but can
modify the effects of neurotransmitters. These chemicals are called neuromodulators.
Identified neurotransmitters and neuromodulators can be divided into two major
categories:
★Small-moleculeTransmitters
Monoamines (eg, Acetylcholine, Serotonin, Histamine),
Catecholamines (Dopamine, Norepinephrine Epinephrine)
Amino Acids (eg, Glutamate, GABA, Glycine).
★Large-molecule Transmitters
Include a large number of peptides called neuropeptides including substance P, enkephalin,
vasopressin, and a host of others.
There are also other substances thought to be released into the synaptic cleft to act as
either a transmitter or modulator of synaptic transmission. These include purine derivatives
like Adenosine, Adenosine Triphosphate (ATP) and Nitric Oxide (NO).
Neurotransmitter receptors
Two broad classes:
★Ligand-gated Ion Channels
Open immediately upon neurotransmitter binding
★G Protein–coupled Receptors.
Neurotransmitter binding to a G protein–coupled receptor induces the opening or closing of
a separate ion channel protein over a period of seconds to minutes. These are “slow”
neurotransmitter receptors.
Each ligand has many subtypes of receptors : selective effect at different sites
Presynaptic receptors, or Autoreceptors : provide feedback control
Receptors are concentrated in clusters in postsynaptic structures close to the endings of
neurons that secrete the neurotransmitters specific for them. This is generally due to the
presence of specific binding proteins for them.
★ln the case of nicotinic acetylcholine receptors at the neuromuscular junction, the protein
is rapsyn
★In the case of excitatory glutamatergic receptors, a family of PB2- binding proteins is
involved.
★GABA(A) receptors are associated with the protein gephyrin, which also binds glycine
receptors, and
★GABA(C) receptors are bound to the cytoskeleton in the retina by the protein MAP-1B.
★★ Acetylcholine ★★
Acetylcholine, which is the acetyl ester of choline, is largely enclosed in small, clear
synaptic vesicles in high concentration in the terminal boutons of cholinergic neurons
• Acetylcholine is the transmitter at the
neuromuscular junction, in autonomic
ganglia,
and
in
postganglionic
parasympathetic
nerve-target
organ
junctions
and
some
postganglionic
sympathetic nerve-target junctions. It is also found within the brain, including the basal
forebrain complex and pontomesencephalic cholinergic complex . These systems may be
involved in regulation of sleep wake states, learning, and memory.
• Cholinergic neurons actively take up choline via a transporter. Choline is also synthesized
in neurons.
•The enzyme choline acetyltransferase is found in high concentration in the cytoplasm of
cholinergic nerve endings. Acetylcholine is then taken up into synaptic vesicles by a
vesicular transporter (VAChT).
• Removed via Hydrolysis to choline and acetate, a reaction catalyzed by the enzyme
ACETYLCHOLINESTERASE.
Acetylcholine Receptors
1. Muscarinic
2. Nicotinic
1. Muscarinic receptors
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Muscarine, the alkaloid responsible for the
toxicity of toadstools, has little effect on
the receptors in autonomic ganglia but
mimics the stimulatory action of acetylcholine on smooth muscle and glands.
These actions of acetylcholine are therefore called muscarinic actions, and the
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receptors involved are muscarinic cholinergic receptors.
They are blocked by the drug atropine.
Five types, encoded by five separate genes, have been cloned.
The exact status of M5 is uncertain, but the remaining four receptors are coupled via
G proteins to adenylyl cyclase, K+ channels, and/or phospholipase C .
M1 is abundant in the brain.
The M2 receptor is found in the heart.
The M4 receptor is found in pancreatic acinar
and islet tissue.
The M3 and M4 reeptors are associated with
smooth muscle.
2. Nicotinic receptors

In Sympathetic Ganglia, the actions of Ach
are unaffected by atropine but MIMICKED BY
NICOTINE. Consequently, these actions of
Ach are nicotinic actions and the receptors
are nicotinic cholinergic receptors.
 Nicotinic receptors are subdivided into those
at neuromuscular junctions and those found
in autonomic ganglia and the central nervous
system
 Both muscarinic and nicotinic acetylcholine
receptors are found in large numbers in the
brain.
 The nicotinic acetylcholine receptors are members of a superfamily of ligand-gated
ion channels
 Each nicotinic cholinergic receptor is made up of five subunits that form a central
channel which, when the receptor is activated, permits the passage of Na+ and other
cations. A prominent feature of neuronal nicotinic cholinergic receptors is their high
permeability to Ca2+.
 The 5 subunits come from a menu of 16 known subunits, α1–α9, β1–β5, γ , δ and ε ,
coded by 16 different genes.
 THE MUSCLE TYPE NICOTINIC RECEPTOR found in the fetus is made up of two α1
subunits, a β1 subunit, a γ subunit, and a δ subunit . In adult,the γ subunit is replaced
by a δ subunit, which decreases the channel open time but increases its
conductance.
 The nicotinic cholinergic RECEPTORS IN AUTONOMIC GANGLIA usually contain α3
subunits in combination with others.
Many of the nicotinic cholinergic receptors in the brain are located presynaptically on
glutamate-secreting axon terminals, and they facilitate the release of this transmitter.
However, others are postsynaptic. Some are located on structures other than neurons, and
some seem to be free in the interstitial fluid, that is, they are perisynaptic in location.
★★ Serotonin ★★
• Serotonin is formed in the body by hydroxylation and decarboxylation of the essential
amino acid TRYPTOPHAN
• Tryptophan hydroxylase in the human CNS is slightly different from the tryptophan
hydroxylase in peripheral tissues, and is coded by a different gene.
SEROTONIN (5-HYDROXYTRYPTAMINE; 5-HT) is
present in highest concentration in blood platelets and
in the gastrointestinal tract, where it is found in the
enterochromaffin cells and the myenteric plexus.
It is also found within the brain stem in the midline
raphé nuclei which project to portions of the
hypothalamus, the limbic system, the neocortex, the
cerebellum, and the spinal cord.
• After release from serotonergic neurons, much of
the released serotonin is recaptured by an active
reuptake
mechanism
and
inactivated
by
MONOAMINE
OXIDASE
(MAO)
to
form
5-hydroxyindoleacetic acid (5-HIAA)
• This substance is the principal urinary metabolite of
serotonin, and its urinary output is used as an index
of the rate of serotonin metabolism in the body.
Serotonergic Receptors
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5-HT1 - 5-HT7 receptors
Most of these are G protein-coupled receptors
5-HT1 => 5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, & 5-HT1F
5-HT2 => 5-HT2A, 5-HT2B, & 5-HT2C
5-HT2A receptors mediate platelet aggregation
and smooth muscle contraction.
5-HT3 receptors are ligand-gated ion channels
present in the GIT & the area postrema & are
related to vomiting.
5-HT4 receptors are also present in the GIT,
where they facilitate secretion and peristalsis, &
in the brain.
5-HT5 => 5-HT5A & 5-HT5B
5-HT6 & 5-HT7 are distributed throughout the
limbic system, and the 5-HT6 receptors have a
high affinity for antidepressant drugs.
★★ Histamine ★★
• Histamine is formed by decarboxylation of the amino acid histidine .
• Histaminergic neurons have their cell bodies in the tuberomammillary nucleus of the
posterior hypothalamus, and their axons project to all parts of the brain, including the
cerebral cortex and the spinal cord.
• Histamine is also found in cells in the gastric mucosa and in heparincontaining cells called
mast cells that are plentiful in the anterior and posterior lobes of the pituitary gland as well
as at body surfaces.
• The three known types of histamine
receptors— H1,H2, and H3—are all found in
both peripheral tissues and the brain.
• Most of the H3 receptors are presynaptic,
and they mediate inhibition of the release
of histamine and other transmitters via a G
protein.
H1
receptors
activate
phospholipase C, and H2 receptors increase the intracellular cAMP concentration.
• Evidence links brain histamine to arousal, sexual behavior, blood pressure, drinking, pain
thresholds, and regulation of the secretion of several anterior pituitary hormones.
★★ Catecholamines ★★
• Norepinephrine, Epinephrine, & Dopamine
•The chemical transmitter present at most sympathetic postganglionic endings is
norepinephrine. It is stored in the synaptic knobs of the neurons that secrete it in
characteristic small vesicles that have a dense core.
• NOREPINEPHRINE and its methyl derivative, EPINEPHRINE, are secreted by the adrenal
medulla.
• Tyrosine hydroxylase, which catalyzes the RATE LIMITING step, is subject to feedback
inhibition by dopamine and norepinephrine, thus providing internal control of the synthetic
process.
• The cell bodies of the norepinephrine-containing neurons are located in the locus ceruleus
and other medullary and pontine nuclei.
Catabolism of Catecholamines
• Removed from the synaptic cleft by binding to
postsynaptic receptors, binding to presynaptic
receptors, reuptake into the presynaptic neurons, or
catabolism.Reupke is a major mechanism in the
case of norepinephrine.
• Epinephrine and norepinephrine are metabolized to
biologically inactive products by oxidation and
methylation. The former reaction is catalyzed by
MAO
and
the
latter
by
catechol
-O
–methyltransferase(COMT).
•
EXTRACELLULAR epinephrine and norepinephrine are
for the most part O-methylated, and measurement of
the concentrations of the O-methylated derivatives
normetanephrine and metanephrine in the urine is a
good index of the rate of secretion of norepinephrine
and epinephrine.
• The O-methylated derivatives that are not excreted
are
largely
oxidized,
and
3-methoxy4-hydroxymandelic acid (vanillylmandelic acid, VMA)
is the most plentiful catecholamine metabolite in the
urine. Small amounts of the O-methylated derivatives
are also conjugated to sulfate and glucuronide.
• In the NORADRENERGIC NERVE TERMINALS, on the
other hand, some of the norepinephrine is constantly
being converted by intracellular MAO to the physiologically inactive deaminated derivatives,
3,4-dihydroxymandelic acid (DOMA) and its corresponding glycol (DHPG). These are
subsequently converted to their corresponding O-methyl derivatives, VMA and 3-methoxy-4
hydroxyphenylglycol (MHPG).
★★ Dopamine ★★
• In certain parts of the brain, catecholamine synthesis stops at dopamine
• Active reuptake of dopamine occurs via a Na+- and
Cl–-dependent dopamine transporter.
• Dopamine is metabolized to inactive compounds
by MAO and COMT in a manner analogous to the
inactivation of norepinephrine
• Dopaminergic neurons are located in several brain
regions including the nigrostriatal system, which
projects from the substantia nigra to the striatum
and is involved in motor control, and the
mesocorticalsystem.
• The mesocortical system projects to the nucleus accumbens and limbic subcortical areas,
and it is involved in reward behavior and addiction.
• Studies by PET scanning in normal humans show that a steady loss of dopamine
receptors occurs in the basal ganglia with age. The loss is greater in men than in women.
Dopamine Receptors
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Five different dopamine receptors have been cloned, and several of these exist in
multiple forms.
Most, but perhaps not all, of the responses to these receptors are mediated by
heterotrimeric G proteins.
Overstimulation of D2 receptors is thought to be related to schizophrenia.
D3 receptors are highly localized, especially to the nucleus accumbens
★★ Glutamate ★★
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The amino acid glutamate is the main excitatory transmitter in the brain and spinal
cord( 75% of the excitatory transmission in the brain.
Glutamate is formed by reductive amination of the Krebs cycle intermediate
α-ketoglutarate in the cytoplasm.
The reaction is reversible, but in glutaminergic neurons, glutamate is concentrated in
synaptic vesicles by the vesicle-bound transporter BPN1.
The cytoplasmic store of glutamine is
enriched by three transporters that import
glutamate from the interstitial fluid, and
two
additional
transporters
carry
glutamate into astrocytes, where it is
converted to glutamine and passed on to
glutaminergic neurons.
Released glutamate is taken up by astrocytes and converted to glutamine, which
passes back to the neurons and is converted back to glutamate, which is released as
the synaptic transmitter.
Uptake into neurons and astrocytes is the main mechanism for removal of glutamate
from synapses.
★★ NMDA ★★
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A cation channel: permits passage of relatively large amounts of Ca2+
Glycine facilitates its function by binding to it, & appears to be essential for its
normal response to glutamate.
When glutamate binds to it, it opens, but at normal membrane potentials, its channel
is blocked by a Mg2+ ion.
Phencyclidine and ketamine, which produce amnesia and a feeling of dissociation
from the environment, bind to another site inside the channel. Most target neurons
for glutamate have both AMPA and NMDA receptors.
Kainate receptors are located presynaptically on Gamma-aminobutyric Acid (GABA)
-secreting nerve endings and postsynaptically at various localized sites in the brain.
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Kainate and AMPA receptors are found
in glia as well as neurons, but it
appears that NMDA receptors occur
only in neurons
The concentration of NMDA receptors
in the hippocampus is high, and
blockade of these receptors prevents
long-term potentiation, a long-lasting
facilitation of transmission in neural
pathways following a brief period of
high-frequency stimulation. Thus, these receptors may well be involved in MEMORY
AND LEARNING.
★★ GABA (Gamma-aminobutyric Acid)★★
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Major inhibitory mediator in the brain, including being responsible for presynaptic
inhibition.
Formed by decarboxylation of
glutamate .The enzyme glutamate
decarboxylase (GAD), is present in
nerve endings in many parts of the
brain.
Metabolized
primarily
by
transamination to succinic semialdehyde and thence to succinate in the citric acid
cycle. GABA transaminase (GABA-T) catalyzes the transamination.
In addition, there is an active reuptake of GABA via the GABA transporter. A vesicular
GABA transporter (VGAT) transports GABA and glycine into secretory vesicles.
GABA Receptors
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Three subtypes of GABA receptors have been identified: GABA(A),GABA(B) and GABA(C)
The GABA(A) and GABA(B) receptors are widely distributed in the CNS, whereas in
adult vertebrates the GABA(C) receptors are found almost exclusively in the retina.
The GABA(A) and GABA(C) receptors are ion channels made up of five subunits
surrounding a pore . In this case,
the ion is Cl–.
Increases in Cl– influx and K+
efflux and decreases in Ca2+
influx all hyperpolarize neurons,
producing an IPSP. The G
protein mediation of GABA(B)
receptor effects is unique in
that a G protein heterodimer,
rather than a single protein, is involved.
There is a chronic low-level stimulation of GABA(A) receptors in the CNS that is aided
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by GABA in the interstitial fluid. This background stimulation cuts down on the
"noise" caused by incidental discharge of the billions of neural units and greatly
IMPROVES THE SIGNAL-TO-NOISE RATIO in the brain. It may be that this GABA
discharge declines with advancing age resulting in a loss of specificity of responses
of visual neurons.
The increase in Cl– conductance produced by GABA(A) receptors is potentiated by
benzodiazepines, drugs that have marked anti-anxiety activity and are also effective
muscle relaxants, anticonvulsants, and sedatives. Benzodiazepines bind to the α
subunits.
At least in part, barbiturates and alcohol also act by facilitating Cl–conductance.
Metabolites of the steroid hormones progesterone and deoxycorticosterone bind to
GABA(A) receptors and increase Cl–conductance.
It has been known for many years that progesterone and deoxycorticosterone are
sleep-inducing and anesthetic in large doses, and these effects are due to their
action on GABA(A) receptors.
★★ Glycine ★★
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Glycine has both excitatory and inhibitory effects in the CNS.
When it binds to NMDA receptors, it makes them more sensitive.It appears to spill
over from synaptic junctions into the interstitial fluid, and in the spinal cord, for
example, this glycine may facilitate pain transmission by NMDA receptors in the
dorsal horn.
Glycine is also responsible in part for
direct inhibition, primarily in the brain stem
and spinal cord. Like GABA, it acts by
increasing Cl–conductance. Its action is antagonized by strychnine.
The clinical picture of convulsions and muscular hyperactivity produced by
strychnine emphasizes the importance of postsynaptic inhibition in normal neural
function.
RECEPTOR
• The glycine receptor responsible for inhibition is a Cl– channel.
• It is a pentamer made up of two subunits:
1. The ligand-binding α subunit
2. The structural β subunit.
• Recently, solid evidence has been presented that three kinds of neurons are responsible
for direct inhibition in the spinal cord:
1. neurons that secrete glycine,
2. neurons that secrete GABA, and
3. neurons that secrete both.
Presumably, neurons that secrete only glycine have the glycine transporter GLYT2, those
that secrete only GABA have GAD, and those that secrete glycine and GABA have both. This
third type of neuron is of special interest because the neurons seem to have glycine and
GABA in the same vesicles.
Large-Molecule Transmitters
Neuropeptides
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Substance P & Other Tachykinins:
Substance P is a polypeptide containing 11 amino acid residues that is found in the
intestine, various peripheral nerves, and many parts of the CNS.
It is one of a family of 6 mammalian polypeptides called tachykinins that differ at the
amino terminal end but have in
common the carboxyl terminal
sequence.
Substance P is found in high
concentration in the endings of
primary afferent neurons in the spinal
cord, and it is probably the mediator
at the first synapse in the pathways
for pain transmission in the dorsal
horn.
It is also found in high concentrations in the nigrostriatal system, where its
concentration is proportional to that of dopamine,and in the hypothalamus, where it
may play a role in neuroendocrine regulation.
In the intestine, it is involved in peristalsis.
Opioid Peptides
Peptides that bind to opioid receptors are called opioid peptides.The ENKEPHALINS are
found in nerve endings in the gastrointestinal tract and many different parts of the brain,
and they appear to function as synaptic transmitters. They are found in the substantia
gelatinosa and have analgesic activity when injected into the brain stem. They also
decrease intestinal motility.
METABOLISM
Enkephalins are metabolized primarily by two peptidases
• Enkephalinase A, which splits the Gly-Phe bond, and
• Enkephalinase B, which splits the Gly-Gly bond.
• Aminopeptidase, which splits the Tyr-Gly bond, also
contributes to their metabolism.
RECEPTORS
•µ,κ,δ
• All three are G protein-coupled receptors, and all
inhibit adenylyl cyclase.
• Activation of µ receptors increases K+ conductance,
hyperpolarizing central neurons and primary afferents. Activation of κ and δ receptors
closes Ca2+ channels.
Other Substances
PROSTAGLANDINS
• Are derivatives of arachidonic acid found in the nervous system, present in nerve-ending
fractions of brain homogenates and are released from neural tissue in vitro. A putative
prostaglandin transporter with 12 membrane-spanning domains has been described.
• However, prostaglandins appear to exert their effects by modulating reactions mediated
by cAMP rather than by functioning as synaptic transmitters.
NEUROACTIVE STEROIDS
• They are not neurotransmitters in the usual sense.
• Evidence has now accumulated that the brain can produce some hormonally active
steroids from simpler steroid precursors, and the term neurosteroids has been coined to
refer to these products. Progesterone facilitates the formation of myelin, but the exact role
of most steroids in the regulation of brain function remains to be determined.
Brain Damage(Disorders)
Parkinson's Disease
Alzheimer's Disease
Parkinson's disease
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Parkinson's disease is a progressive nervous system disorder that affects
movement. Symptoms start gradually, sometimes starting with a barely noticeable
tremor in just one hand. Tremors are common, but the disorder also commonly
causes stiffness or slowing of movement.
In the early stages of Parkinson's disease, your face may show little or no expression.
Your arms may not swing when you walk. Your speech may become soft or slurred.
Parkinson's disease symptoms worsen as your condition progresses over time.
Although Parkinson's disease can't be cured, medications might significantly
improve your symptoms. Occasionally, your doctor may suggest surgery to regulate
certain regions of your brain and improve your symptoms.
Symptoms
Parkinson's disease signs and symptoms can be different for everyone. Early signs may be
mild and go unnoticed. Symptoms often begin on one side of your body and usually remain
worse on that side, even after symptoms begin to affect both sides.
Parkinson's signs and symptoms may include:
1. Tremor. A tremor, or shaking, usually begins in a limb, often your hand or fingers.
You may rub your thumb and forefinger back and forth, known as a pill-rolling tremor.
Your hand may tremble when it's at rest.
2. Slowed movement (bradykinesia). Over time, Parkinson's disease may slow your
movement, making simple tasks difficult and time-consuming. Your steps may
3.
4.
5.
6.
7.
become shorter when you walk. It may be difficult to get out of a chair. You may drag
your feet as you try to walk.
Rigid muscles. Muscle stiffness may occur in any part of your body. The stiff
muscles can be painful and limit your range of motion.
Impaired posture and balance. Your posture may become stooped, or you may have
balance problems as a result of Parkinson's disease.
Loss of automatic movements. You may have a decreased ability to perform
unconscious movements, including blinking, smiling or swinging your arms when you
walk.
Speech changes. You may speak softly, quickly, slur or hesitate before talking. Your
speech may be more of a monotone rather than have the usual inflections.
Writing changes. It may become hard to write, and your writing may appear small.
Pathophysiology
Antipsychotic drugs , encephalitis and other causes
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Affects the substantia nigra
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Destuction of dopamine producing neurons within the basal ganglia
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Reduces the amount of available straital dopamine ( inhibitory effects )
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There is increase in acetylcholine (excitatory effects )
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Excitatory activity of Ach is inadequately balanced
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Difficulty in controlling and initiating voluntary movements
Causes
In Parkinson's disease, certain nerve cells (neurons) in the brain gradually break down or die.
Many of the symptoms are due to a loss of neurons that produce a chemical messenger in
your brain called dopamine. When dopamine levels decrease, it causes abnormal brain
activity, leading to impaired movement and other symptoms of Parkinson's disease.
০ The cause of Parkinson's disease is unknown, but several factors appear to play a role,
including:
 Genes. Researchers have identified specific genetic mutations that can cause
Parkinson's disease. But these are uncommon except in rare cases with many family
members affected by Parkinson's disease.
 However, certain gene variations appear to increase the risk of Parkinson's disease
but with a relatively small risk of Parkinson's disease for each of these genetic
markers.
 Environmental triggers. Exposure to certain toxins or environmental factors may
increase the risk of later Parkinson's disease, but the risk is relatively small.
০ Researchers have also noted that many changes occur in the brains of people with
Parkinson's disease, although it's not clear why these changes occur. These changes
include:
 The presence of Lewy bodies. Clumps of specific substances within brain cells are
microscopic markers of Parkinson's disease. These are called Lewy bodies, and
researchers believe these Lewy bodies hold an important clue to the cause of
Parkinson's disease.
 Alpha-synuclein found within Lewy bodies. Although many substances are found
within Lewy bodies, scientists believe an important one is the natural and
widespread protein called alpha-synuclein (a-synuclein). It's found in all Lewy bodies
in a clumped form that cells can't break down. This is currently an important focus
among Parkinson's disease researchers.
Risk factors
Risk factors for Parkinson's disease include:
1. Age. Young adults rarely experience Parkinson's disease. It ordinarily begins in
middle or late life, and the risk increases with age. People usually develop the
disease around age 60 or older.
2. Heredity. Having a close relative with Parkinson's disease increases the chances
that you'll develop the disease. However, your risks are still small unless you have
many relatives in your family with Parkinson's disease.
3. Sex. Men are more likely to develop Parkinson's disease than are women.
4. Exposure to toxins. Ongoing exposure to herbicides and pesticides may slightly
increase your risk of Parkinson's disease.
Complications
০ Parkinson's disease is often accompanied by these additional problems, which may be
treatable:
 Thinking difficulties. You may experience cognitive problems (dementia) and
thinking difficulties. These usually occur in the later stages of Parkinson's disease.
Such cognitive problems aren't very responsive to medications.
 Depression and emotional changes. You may experience depression, sometimes in
the very early stages. Receiving treatment for depression can make it easier to
handle the other challenges of Parkinson's disease.
০ You may also experience other emotional changes, such as fear, anxiety or loss of
motivation. Doctors may give you medications to treat these symptoms.
 Swallowing problems. You may develop difficulties with swallowing as your
condition progresses. Saliva may accumulate in your mouth due to slowed
swallowing, leading to drooling.
 Chewing and eating problems. Late-stage Parkinson's disease affects the muscles
in your mouth, making chewing difficult. This can lead to choking and poor nutrition.
 Sleep problems and sleep disorders. People with Parkinson's disease often have
sleep problems, including waking up frequently throughout the night, waking up early
or falling asleep during the day.
০ People may also experience rapid eye movement sleep behavior disorder, which involves
acting out your dreams. Medications may help your sleep problems.
 Bladder problems. Parkinson's disease may cause bladder problems, including being
unable to control urine or having difficulty urinating.
 Constipation. Many people with Parkinson's disease develop constipation, mainly
due to a slower digestive tract.
০ You may also experience:
 Blood pressure changes. You may feel dizzy or lightheaded when you stand due to a
sudden drop in blood pressure (orthostatic hypotension).
 Smell dysfunction. You may experience problems with your sense of smell. You may
have difficulty identifying certain odors or the difference between odors.
 Fatigue. Many people with Parkinson's disease lose energy and experience fatigue,
especially later in the day. The cause isn't always known.
 Pain. Some people with Parkinson's disease experience pain, either in specific areas
of their bodies or throughout their bodies.
 Sexual dysfunction. Some people with Parkinson's disease notice a decrease in
sexual desire or performance.
Prevention
Because the cause of Parkinson's is unknown, proven ways to prevent the disease also
remain a mystery.
Some research has shown that regular aerobic exercise might reduce the risk of
Parkinson's disease.
Some other research has shown that people who consume caffeine — which is found in
coffee, tea and cola — get Parkinson's disease less often than those who don't drink it.
Green tea is also related to a reduced risk of developing Parkinson's disease. However, it is
still not known whether caffeine actually protects against getting Parkinson's, or is related
in some other way. Currently there is not enough evidence to suggest drinking caffeinated
beverages to protect against Parkinson's.
Alzheimer's disease
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Alzheimer's disease is a progressive disorder that causes brain cells to waste away
(degenerate) and die. Alzheimer's disease is the most common cause of dementia —
a continuous decline in thinking, behavioral and social skills that disrupts a person's
ability to function independently.
The early signs of the disease may be forgetting recent events or conversations. As
the disease progresses, a person with Alzheimer's disease will develop severe
memory impairment and lose the ability to carry out everyday tasks.
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Current Alzheimer's disease medications may temporarily improve symptoms or
slow the rate of decline. These treatments can sometimes help people with
Alzheimer's disease maximize function and maintain independence for a time.
Different programs and services can help support people with Alzheimer's disease
and their caregivers.

There is no treatment that cures Alzheimer's disease or alters the disease process in
the brain. In advanced stages of the disease, complications from severe loss of brain
function — such as dehydration, malnutrition or infection — result in death.
Symptoms
Memory loss is the key symptom of Alzheimer's disease. An early sign of the disease is
usually difficulty remembering recent events or conversations. As the disease progresses,
memory impairments worsen and other symptoms develop.
At first, a person with Alzheimer's disease may be aware of having difficulty with
remembering things and organizing thoughts. A family member or friend may be more likely
to notice how the symptoms worsen.
Brain changes associated with Alzheimer's disease lead to growing trouble with:
Memory
Everyone has occasional memory lapses. It's normal to lose track of where you put your
keys or forget the name of an acquaintance. But the memory loss associated with
Alzheimer's disease persists and worsens, affecting the ability to function at work or at
home.
People with Alzheimer's may:
 Short term memory loss – forgetting recent events, names and places
 Difficulty performing familiar tasks
 Disorientation especially away from your normal surroundings
 Increasing problems with planning and managing
 Trouble with language
 Rapid, unpredictable mood swings
 Lack of motivation
 Changes in sleep and confusion about the time of day
 Reduced judgement e.g. being unaware of danger
Alzheimer's disease causes difficulty concentrating and thinking, especially about abstract
concepts such as numbers.
Multitasking is especially difficult, and it may be challenging to manage finances, balance
checkbooks and pay bills on time. These difficulties may progress to an inability to
recognize and deal with numbers.
Making judgments and decisions
The ability to make reasonable decisions and judgments in everyday situations will decline.
For example, a person may make poor or uncharacteristic choices in social interactions or
wear clothes that are inappropriate for the weather. It may be more difficult to respond
effectively to everyday problems, such as food burning on the stove or unexpected driving
situations.
Planning and performing familiar tasks
Once-routine activities that require sequential steps, such as planning and cooking a meal
or playing a favorite game, become a struggle as the disease progresses. Eventually, people
with advanced Alzheimer's may forget how to perform basic tasks such as dressing and
bathing.
Changes in personality and behavior
Brain changes that occur in Alzheimer's disease can affect moods and behaviors. Problems
may include the following:
 Depression
 Apathy
 Social withdrawal
 Mood swings
 Distrust in others
 Irritability and aggressiveness
 Changes in sleeping habits
 Wandering
 Loss of inhibitions
 Delusions, such as believing something has been stolen
 Preserved skills
Many important skills are preserved for longer periods even while symptoms worsen.
Preserved skills may include reading or listening to books, telling stories and reminiscing,
singing, listening to music, dancing, drawing, or doing crafts.
These skills may be preserved longer because they are controlled by parts of the brain
affected later in the course of the disease.
Causes
Scientists believe that for most people, Alzheimer's disease is caused by a combination of
genetic, lifestyle and environmental factors that affect the brain over time.
Less than 1 percent of the time, Alzheimer's is caused by specific genetic changes that
virtually guarantee a person will develop the disease. These rare occurrences usually result
in disease onset in middle age.
The exact causes of Alzheimer's disease aren't fully understood, but at its core are
problems with brain proteins that fail to function normally, disrupt the work of brain cells
(neurons) and unleash a series of toxic events. Neurons are damaged, lose connections to
each other and eventually die.
The damage most often starts in the region of the brain that controls memory, but the
process begins years before the first symptoms. The loss of neurons spreads in a
somewhat predictable pattern to other regions of the brains. By the late stage of the
disease, the brain has shrunk significantly.
Researchers are focused on the role of two proteins:
Plaques. Beta-amyloid is a leftover fragment of a larger protein. When these fragments
cluster together, they appear to have a toxic effect on neurons and to disrupt cell-to-cell
communication. These clusters form larger deposits called amyloid plaques, which also
include other cellular debris.
Tangles. Tau proteins play a part in a neuron's internal support and transport system to
carry nutrients and other essential materials. In Alzheimer's disease, tau proteins change
shape and organize themselves into structures called neurofibrillary tangles. The tangles
disrupt the transport system and are toxic to cells.
Cure and Treatment for Alzheimer’s
★Currently there is no cure for Alzheimer’s. However there are several drugs that may be
prescribed to help people with Alzheimer’s. They are not a cure, but can help with some of
the symptoms of the disease.
★Drugs such as donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) are
used to treat symptoms in Alzheimer's disease.
★Antidepressants, anti-anxiety medications, and anti-psychotics are used to treat the
symptoms of depression,anxiety,agitation and the hallucinations and delusions that may
occur in Alzheimer's disease patients
EMOTION
• Emotion is a complex psychological phenomenon which occurs as animals or people live
their lives.
• It is Intense feeling that are directed at someone or something
•Emotions are our body’s adaptive response.
Emotions Include Three Things
• conscious experience (feelings)
• expressions which can be seen by others
• actions of the body ('physiological arousal')
Emotions Are Divided Into Two Categories
• Primary Emotions
• Secondary Emotions
Human Emotion
• Human emotion is innate in all of us; it’s something we’re born with and something we die
with.
• Happiness, sadness, love, hatred, worries, and indifference – these are things that
constantly occur in our daily lives.
Variety Of Emotions
• Positive Human Emotion (PHE)
• Negative Human Emotion (NHE)
Positive emotion
Positive emotions that lead one to feel good about one’s self will lead to an emotionally
happy and satisfied result.
Negative emotion
Negative emotions sap your energy and undermine your effectiveness. In the negative
emotional state, you find the lack of desire to do anything.
Factors Affecting Emotions
PERSONALITY
CULTURE
WEATHER
STRESS
AGE
GENDER
ENVIROMENTAL
Embodied Emotion
★Emotions and The Autonomic Nervous System
★Physiological Similarities Among Specific
Emotions
★Physiological Differences Among Specific
Emotions
★Thinking Critically About: Lie Detection
★Cognition And Emotion
Expressed Emotion
★Nonverbal Communication
★Detecting and Computing Emotion
★Culture and Emotional Expression
★The Effects of Facial Expression
Experienced Emotion
★Fear
★Anger
★Happiness
Analyzing Emotion
Analysis of emotions are carried on different levels.
Theories of Emotion
Dimensions of Emotion
People generally divide emotions into two dimensions.
Emotional Ups and Downs
Our positive moods rise to a maximum within 6-7 hours after waking up. Negative moods
stay more or less the same throughout the day.
Predictors of Happiness
Why are some people generally more happy than others?