psychobiology Flashcards
1
Q
what are the three fundamental assumptions in psychobiology?
A
- behaviour is dependent upon body function
- the brain is the primary body area involved
- try not to completely neglect the role of other body areas
2
Q
what is dualism?
A
cartesian duality - the belief that both physical and mental substance is fundamental
3
Q
what is physicalism (monism)?
A
matter> mind
physical substances are more fundamental to a persons psychology
4
Q
what is idealism (monism)?
A
mind> matter
mental substances are more fundamental to a persons psychology
5
Q
what is neutral monism?
A
a hypothetical third substance is fundamental to a persons psychology, physical and mental substances are derivative to this.
6
Q
what is reductionism?
A
when a phenomenon is defined in terms of the more elementary processes that underlie it (simplifies it)
7
Q
what are the three levels of reductionism?
A
macro anatomical level (largest) - functional interaction of different brain areas
micro anatomical level - functional interaction of different brain cells
macro molecule level (smallest) - functional interaction of individual protein molecules
8
Q
what is a cell?
A
fundamental building block of all biological organisms generated by mitosis followed by differentiation
9
Q
what is the brain?
A
neurones, information processing and transmitting element of nervous system
10
Q
what is glia?
A
supporting cells, has functions that neurones cannot do
11
Q
name the characteristics of a neurone?
A
- fully differentiated
- cannot undergo mitosis
- typically can’t be replaced in mature nervous systems but can be regenerated in certain parts of the brain throughout our life
- tumours of neurones are very rare
12
Q
what is the cell body?
A
(soma) integrates information
13
Q
what are dendrites?
A
(dendritic tree) branch like processes on the cell body, receives information from other neurones
14
Q
what is an axon?
A
(typically myelinated to speed up transmissions) long filament like process, branches, conveys information away from the cell body to other neurones that end in terminals
15
Q
what is a synapse?
A
a gap between the pre and postsynaptic neurone that connects one terminal to another
16
Q
does communication with and between neurones need to be slow or fast?
A
fast, specifically for reflexes
17
Q
what kind of process are signals?
A
electric, this is because it is not via diffusion of chemicals as that would be too slow
18
Q
what is resting membrane potential an example for?
A
electrical excitability
19
Q
what is electrical excitability?
A
describes the potential movement of particles if allowed
20
Q
what occurs when a neurone is in a passive state?
A
energy is being spent/used up in order to maintain an unstable state
21
Q
what occurs to a neurone in an unstable state when a trigger occurs?
A
the pent up energy is released which creates the signal/action potential
22
Q
what does the resting membrane potential depend on and why?
A
the fact that the cell membrane of a neurone is a lipid (fatty layer) which makes charged ions unable to pass through easily
23
Q
what within the cell membrane acts as an ion transporter for sodium and potassium?
A
proteins
24
Q
describe the transportation of sodium and potassium ions
A
more sodium ions are moved outside of the membrane where in exchange potassium ions are moved inside the membrane.
25
what charges are sodium and potassium?
single positive charges
26
what are cations?
+vely charged ions
27
what are anions?
-vely charged ions
28
what are chloride ions?
chloride ions are anions (-ve) and do not leak through the membrane
29
what is the resting membrane potential difference?
-70mV
30
what is the myelin sheath?
made from oligodendrocytes and insulates neurones and speeds up action potential as well as blocking interference from other neurotransmitters
31
what are nodes of ranvier?
they are spaces between myelinated sections of the axon
32
'action potentials are the basic code for information in the brain'
what are the characteristics of this code?
AP's are always the same size and shape
they either occur or do not
size of AP holds no information
frequency (rate) of AP's codes information
33
does an action potential increase or decrease as it travels underneath the myelin sheath?
decreases due to the insulating properties
34
as action potential jumps between nodes what occurs?
full action potential is regenerated at nodes between the myelinated axons which saves energy
35
what do sensory receptors do?
respond to sensory stimulation directly with membrane depolarisation
36
what are the three main neurotransmitters in synaptic transmission and plasticity?
Glutamate
GABA
Monoamines
37
what are the three main receptors in synaptic transmission and plasticity?
Ionotropic
Metabotropic
Selective binding
38
what is a ligand?
a ligand is a chemical that interacts with the receptors, an example is a neurotransmitter
39
what do ligands interact with?
the binding site on receptors
40
what are the characteristics of selectivity of binding?
- only specific ligands will fit in a binding site
- due to the 3D shape of the receptor
- but some drugs bind to more than one receptor type
41
what is affinity?
how well a ligand binds to a receptor
42
what does a high affinity mean?
that receptors are saturated (completely bound) by very dilute solutions of ligands
43
what does a synaptic transmission produce?
a small postsynaptic potential
44
what are the characteristics of an ionotropic receptor?
- directly coupled to an ion channel
- ligand binds -> ion channel opens
45
how does a metabotropic receptor work?
- more complex
- ligand binds and changes 3D shape of the receptor
- this activates a G-protein that is connected to the receptor inside the neurone
- this activates an intracellular signalling cascade
- can either alter ionotropic receptors to make them more or less excitable or can alter protein synthesis
46
what are two amino acid derivatives?
glutamate and GABA
47
what are the characteristics of glutamate?
derived from glutamic acid
most abundant neurotransmitter
excitatory
binds to at least 8 different receptors
48
what are the characteristics of GABA?
Gamma-aminobutyric acid
made from glutamate
most abundant inhibitory neurotransmitter
binds to both ionotropic and metabotropic GABA receptors
49
what influences the probability of an action potential firing?
post synaptic neurones integrating across many inputs
50
what size are post synaptic potentials?
they are very small as the opening of a single channel is insufficient to produce enough hyperpolarization to alter action potential rates
51
what is LTP?
Long term potentiation, a process involving persistent strengthening of synapses that leads to a long lasting increase in signal transmission between neurones
52
what occurs in NMDA receptors for induction?
Magnesium block, depolarisation removes the block, calcium entry into postsynaptic neurone, blocking NMDA receptors impairs the induction of LTP
53
what occurs in AMPA receptors for expression?
more AMPA receptors, larger excitatory post synaptic potential (glutamate binding to more receptors), more glutamate release
54
what is learning?
acquisition of behavioural information
55
what is memory?
the retention of information
56
what is a principle of learning?
memory gets better with more learning
57
what is the law of diminishing returns?
states the continuous equal effort of learning results in less additional improvement or benefit
58
what is the role of surprise in learning?
the amount of knowledge is proportional to the amount of surprise at the outcome
59
what is the rescorla-wagner rule of learning?
∆V = αβ(λ − ΣV)
60
explain the rescorla-wagner rule
the change in the level of memory = speed we learn about the environment and predictors of the outcome X speed we learn about the outcomes (maximum that can be learnt/asymptote - what is already known before any learning)
61
explain what blocking is
blocking describes a situation where there is two stimuli, one of which blocks the learning of the other due to its predictive value.
62
what is pharmacokinetics?
routes of drug administration
63
what is pharmacodynamics?
examples of agonists, antagonists and allosteric modulators
64
what is quantifying drug effects?
efficacy and potency
65
what are psychoactive drugs?
(psychotopric) drugs which alter your transmission to affect a mood or behaviour, they can be found in plants or compounds that have been synthesised in a chemical laboratory
66
what are the 6 routes of adminstration?
1. oral (ingestion)
2. rectal (anus)
3. other mucous membranes:
sublingual, buccal and nasal
4. transdermal
5. inhalation
6. injection: intravenous, intramuscular and subcutaneous
67
what is sublingual?
under the tongue
68
what is buccal?
inside the cheek
69
what is intravenous?
into the vein
70
what is intramuscular?
into the muscle
71
what is subcutaneous?
into the skin
72
where does absorption via oral administration often occur?
small intestines
73
what is the rate of oral administration?
slow
74
when is it best to take oral administration?
on an empty stomach
75
name advantages of oral adminstration
easy
allows for drug to be out of the system
limited infection risk
76
name disadvantages for oral administration
stomach is very acidic so some drugs may be broken down
foodstuffs in guts can make absorption unpredictable
some drugs irritate the stomach and induce vomiting
blood supply from gut routed to liver so first pass effect may occur and prevents the whole drug to reach circulation
77
what is the first pass effect?
liver metabolism breaks down active drugs to metabolites for elimination, the first pass effect is the extent to which a drug is metabolised by the liver before reaching systemic circulation. from the GI tract, drugs pass via the portal vein into the liver. the result of first pass metabolism means that only a proportion of the drug reaches the circulation.
78
name advantages of rectal administration
can be used if person is vomiting or unconscious
79
name disadvantages of rectal administration
unpredictable rate of absorption
not well accepted by some
80
name advantage of other mucous membranes
avoid first pass metabolism
81
name a disadvantage of other mucous membranes
all relatively slow compared with inhalation/injections
82
name the steps of drug administration
absorption
distribution
metabolism
elimination
83
briefly describe how absorption occurs
unless given via intravenous, a drug must cross cell membranes before it can get round the body in blood plasma
84
what are the factors that affect diffusion of drugs across lipid membranes?
- lipid-soluble and small molecules drugs diffuse the best
- un-ionised drug molecules are more lipid soluble
85
do drugs know where to go within the body?
they don't, drugs circulate throughout the body in plasma then enter tissue sites, they encounter receptors for which they have affinity, bind and begin the pharmacological response
86
what occurs during distribution?
the target for psychoactive drugs is usually the brain but in blood plasma a drug will reach all parts of the body
87
why do side effects occur for psychoactive drugs?
they can be due to binding at receptors outside the brain.
88
why do some drugs get temporarily inactivated?
by storage in fat or attached to blood plasma proteins , the blood brain barrier acts as a selective barrier to drug distribution
89
what occurs during metabolism?
converts the drug chemically into another compound, this can be inert and can also be active or even more active. this mainly takes place in liver contains enzymes that help metabolism
90
what are the different routes of elimination?
urine
breath
sweat and hair
91
how do drugs get eliminated via urine?
via the kidneys but this is only possible for water-soluble compounds, fat-soluble drugs may be metabolised to make them water-soluble
92
what is drug half life?
half life is a measure of duration of drug action aka time taken for amount of drug in plasma to fall by 50%. this impacts how frequently a drug has to be taken
93
name the characteristics of transdermal patches
controlled release from a reservoir through a membrane, long duration of action, potential for allergic reactions to the patch or adhesives. drug must be potent or else patches needed are too large, sweat and moisture may lift the patch
94
name the characteristics of inhalation
gases, aerosols, smoke. it is very fast, gases can leave and enter lungs quickly and can cause damage to lungs
95
name the characteristics of injection (IV)
very fast, allows accuracy in dose, can cause clots/infection
96
name the characteristics of intramuscular
not as fast as IV or inhalation but faster than others
97
name characteristics of subcutaneous
drug diffuses into area between skin and muscle, slowest form of injection, can only inject small volumes
98
what are the factors affecting choice of route of administration
ease of administration
desired onset and duration of action
quantity of drug to be administered
balance of risk versus benefits
99
how do psychoactive drugs bring about their effects?
most drugs that affect behaviour alter chemical neurotransmission (agonist) , can either enhance the effects of a neurotransmitter or dampen or block the effects of a neurotransmitter (antagonist)
100
what is a direct agonist?
mimics effects of a neurotransmitter by binding to postsynaptic receptors in a similar way and producing a similar postsynaptic response
101
what is an indirect agonist?
enhances the action of a natural neurotransmitter
102
what is a direct antagonist drug?
binds to a receptor but has NO physiological effect at that receptor e.g naloxone which blocks opioid receptors
103
what is an indirect antagonist drug?
dampens neurotransmitter activity by inhibiting the release/production of neurotransmitters e.g reserpine - reduces transport of monoamines into storage vesicles in neurone terminals
104
how can direct antagonists be classified as?
'full' or 'partial' agonists
depending on the extent to which they mimic the effects of the endogenous neurotransmitter
105
what is an inverse agonist drug?
produces the opposite physiological changes to an agonist
106
what is allosteric modulation?
a chemical (modulator) binds to a different part of the receptor than the neurotransmitter and by doing so alters the receptors response to the neurotransmitter
107
what is the quantifying drug effect?
the magnitude of a drug-receptor effect depends on its concentration at the target site and the affinity of the drug for the receptor site. this can be quantified by a dose-response curve
108
what is ED50?
a measure of potency, the amount of drug required to produce a specific effect indicates potency and Ed50 is the dose producing half the maximal effect
109
describe the difference between efficacy and potency
a potent drug is not necessarily the most clinically effective, a drug can be potent without being efficacious. an efficacious drug might not be very potent but this is only a problem if giving it in a large dose is problematic
110
what is memory consolidation?
when acquisition leads to the long term memory store
111
what is de novo protein synthesis?
the formation/making of new proteins within neurones in the brain
112
what are specific proteins?
proteins that are needed to be made in order for these memories to consolidate within the amygdala
113
give an example of a specific protein
ARC
114
are more or less proteins expected with more learning
more amount of specific protein
115
what is a NMDA receptor?
a receptor of glutamate, the primary excitatory neurotransmitter in the human brain
116
what happens when NMDA receptors are blocked?
LTM is gone and STM is impaired meaning they are required for memory acquisition
117
what are the three factors contributing to differences in drug effects?
individual differences
experience
context
118
explain how individual differences contribute to differences in drug effects
person related factors and environmental influences may influence the response to a drug outside of dose administration
119
what are kinetic differences?
for same doses, a different amount of drug reaches site of action
120
what are pharmacodynamic differences?
for same drug concentrations at site of action, different physiological responses occur
121
what is an idiosyncratic response?
person may experience an atypical drug reaction such as hypersensitivity, hyposensitivity and allergic reaction
122
what might an idiosyncratic response reflect?
reflect genetics, prior exposure to viruses or toxins etc
123
what are the 5 factors contributing to differences in drug effects between people?
body size
age
health
sex
ethnicity/race
124
describe how body size may cause differences in drug effects between people
the same dose produces a smaller response in a larger person as drug is distributed in greater blood volume so would require a larger dose
125
describe how age may cause differences in drug effects between people?
metabolism - liver may be less able to metabolise many drugs as with age comes a decrease in liver function and liver mass is reduced
excretion - kidneys are less able to excrete drugs into the urine
drug-disease and drug drug interactions - chronic disease states and the use of multiple medications may have an effect
compliance - 40% of older people do not take drugs as directed
126
describe how sex may cause differences in drug effects between people
compared with men, women have on average lower plasma volume, higher proportion of body fat, differences in drug response according to phase of menstrual cycle and metabolise some drugs differently
127
describe what biotransformation of alcohol is?
alcohol is first metabolised by the enzyme alcohol dehydrogenase. this enzyme converts alcohol into the metabolite acetaldehyde, a steady amount of approx 10ml of 100% ethanol can be metabolised per hour
128
describe the first stage of the metabolism of alcohol
Alcohol (alcohol dehydrogenase, enzyme in liver and stomach) —-> acetaldehyde (highly reactive and toxic)
129
describe the second stage of the metabolism of alcohol
Acetaldehyde —-> acetic acid —-> oxidised to CO2 and H2O (yields energy)
130
describe how presence of food in the stomach may cause differences in the metabolism of alcohol between people
drinking on a full stomach retains alcohol in the stomach for longer so that more is metabolised by gastric alcohol dehydrogenase
131
how does sex may cause differences in the metabolism of alcohol between people
on average, equivalent amounts of alcohol have greater effect on women than on men as men have a greater vascular capacity, greater body mass on average, alcohol more diluted in blood of men, men have higher levels of gastric alcohol dehydrogenase so less alcohol will get into the blood of men
132
how and why might responses to alcohol or nicotine vary according to a person's racial/ethnic group?
genetics, some genetics differences map onto racial/ethnic groups and affect drug response i.e. how a person responds to the drug itself however race/ethnicity is not a perfect marker for these genetic differences. genetic ancestry may be more relevant than a person's self identified race
133
what are the different kinds of tolerance?
metabolic tolerance - typically, the drug is metabolised faster with repeated use as some drugs induce enzymes in the liver which contributes to their biotransformation
cellular tolerance - neurones adjust their functioning to compensate for the action of the drug on the cell e.g change amount of transmitter synthesised or released, or change number of receptors
sensitisation - response to drug increases over time, opposite of tolerance and common for stimulant drugs
134
explain placebos effects
a placebo is a drug that lacks any intrinsic pharmacological activity (i.e. it is pharmacologically inert) and can produce effects that are indistinguishable from a "real" drug: both behavioural and physiological. in addition to this, expectancies of specific effects have an effect on effectiveness of drugs
135
what does psychoactive mean?
whether it will effect the brain or not
136
what is compliance?
how often does it have to be taken
137
what does ED mean?
effective dose
138
what does LD mean?
lethal dose
139
how does the blood brain barrier work?
blood brain barrier separates the brain from the body and is really small/thin. things can only travel through either between the cells or directly through the cell.
140
why is the amygdala important for the fear emotional response?
amygdala target areas control responses that make up the biological component of the fear emotional response and is ideally-placed to be a key node in emotional responses
141
what lobe is the prefrontal lobe placed in?
frontal
142
what do people believe the pre frontal cortex is responsible for?
emotional decision making
143
what are the three findings of functional studies in PFC?
1. decreased activity of PFC in young people with history of violent behaviour
2. decreased activity of PFC in murderers and increased activity of amygdala
3. vPFC is not specific to anger/aggression; inhibits other emotional states
144
what is memory extinction?
the process that underlies the reduction of a conditioned response when the conditioned stimulus no longer predicts the unconditioned stimulus
145
once memory extinction occurs can the memory resurface?
yes, the memory can recover and resurface
146
what is the PAG?
periaqueductal grey
147
where is the PAG located?
around the central aqueduct deep in the brain
148
what are the steps of emotional regulation?
PFC inhibits amygdala (keeps it under control), the amygdala then activates PAG, through that the amygdala can coordinate the biological response
149
what is the interim summary on emotion?
emotions are the result of complex two way interactions between physiological state and cognitive processes
150
what system is involved in emotion?
limbic
151
what is the amygdala involved with concerning emotion?
attributes emotional significance to events
152
what is the ventral PFC involved with concerning emotion?
emotional decision making
153
what is the PAG is involved with concerning emotion?
the selection of defensive emotional responses
154
what are emotions driven by?
biologically significant stimuli
155
what are the adaptive benefits of emotions?
find food/water/mates
avoid danger
signal
156
how can emotions be maladaptive?
phobias
PTSD
drug addiction/non-homeostatic obesity
157
what do emotional facial expressions signal?
internal state
158
during what time are facial expression more readily observed?
social situations
158
are facial expressions alone sufficient in determining the internal state?
no
159
what 6 expressions are consistently identified?
anger
sadness
happiness
fear
disgust
surprise
160
are emotional facial expressions global?
there are social cultural differences in terms of facial expressions
161
what is the amygdalas involvement in recognition of emotional facial expressions?
damage to the amygdala impairs recognition of emotional facial expressions but does not affect ability to recognise identity nor recognition of emotion from tone of tone
162
what can amygdala patients do to recognise emotional expressions?
can be trained
163
which side of the brain/face is more expressive?
left side of the face
right side of the brain
164
what is activation in dorsolateral PFC and anterior cingulate associated with?
associated with attempts to control unwanted prejudicial responses to black faces
165
what is white matter?
it is composed of myelinated axons and provides connections between different cortical regions
166
what are these connections essential for?
cognitive function
167
what does the variability in white matter underlie?
individual differences in our cognitive abilities
168
what does white matter damage result in?
in the breakdown of connectivity which leads to cognitive deficits such as disconnection syndrome
169
what is essential to brain development and maturation?
white matter changes and strengthening of connections between different cortical regions
170
what are some neurodevelopmental disorders a result of?
of abnormal connectivity
171
does white matter change?
white matter changes as we learn or practise new skills (brain plasticity)
172
what is used to non-invasively study white matter and connectivity in the human brain?
brain imaging techniques, DTI (diffusion tensor imaging) and tractography
173
what is incentive motivation?
behaviour is drawn towards rewards e.g food
174
what is incentive value referring to?
the value of rewards depends upon current drive state e.g food not as attractive when full
175
what signals do insulin produce?
signals relating to nutritional state
176
what signals do dopamine produce?
signals relating to food reward
177
what reduces appetite in women?
intranasal insulin
178
what is the DSM-5 definition of PTSD?
triggered by exposure to actual or threatened death, serious injury or sexual violation and causes clinically significant distress or impairment in the individuals social interactions, capacity to work or other important areas of functioning
179
what are the 4 diagnostic clusters of PTSD?
re-experiencing (flashbacks)
avoidance (avoiding triggers or reminders of their trauma)
negative cognitions (low moods or depression)
arousal (more responsive or reactive to stimulation)
180
what did activation of the amygdala correlate with in PTSD patients?
symptom severity
181
what is the correlation between activity in amygdala and PFC?
negative
182
what happens to cortisol in PTSD?
it is reduced
183
what does enhanced noradrenaline do to traumatic memories?
potentiate (increase the effect)
184
how does cortisol and NA compete with eachother?
low cortisol -> high NA
185
what is NA important for?
emotional memories
186
what may prevent PTSD?
attenuating (reducing the effect) of NA
187
extinction is known to depend upon the ___
PFC
188
what might impaired PFC function result in?
weaker extinction and so enhanced persistence of traumatic memory
189
what are PTSD patients impaired at?
fear memory extinction
190
what is consummatory behaviour?
stereotyped/reflexive= hypothalamus
191
what is preparatory behaviour?
flexible/goal-directed=amygdala
192
what is homeostasis?
the maintenance of an ideal, stable physiological environment where deviation s from the ideal result in a need state or physiological deprivation state
193
what does a need or physiological deprivation
state result in?
a psychological state called drive state where the drive activates and directs behaviour
194
what is the homeostatic theory?
early homeostatic drive explanations of behaviour suggest that the body detects a deviation from a physiological set point. when the set point is restored the body sends out a signal to stop acting which is an example of a negative feedback system.
195
what is hedonic reward?
unrelated to motivational drive, rewarding properties of stimuli alter behaviour
196
what is liking?
liking = sensory pleasure (unconscious)
can be conditioned
brainstem
hierarchal control
197
what is wanting?
wanting = motivational incentive value
not sensory pleasure
not cognitive
can also be conditioned to stimuli
mesolimbic dopamine
198
describe the formation of the nervous system
neural plate closes
it is pulled down to create a neural groove with neural folds
BMP releases neural crest cells
199
what is proliferation?
rapid cell divisions regardless of cell type, neurogenesis refers to birth of neurones
200
what is neurogenesis?
neuronal proliferation as it leads to exponential increase in the number of new neurones (adult isn't as fast)
201
what is neural migration?
neurones begin to migrate from where they were produced to start forming our cerebral cortex
202
what is specific neuroanatomy?
six layered cerebral cortex
subcortical structures
connectivity
203
what is axonal formation and synaptogenesis?
as axons begin to form, synapses start to grow which is the early stages of connectivity
204
what is neuronal and circuits refinement?
sometimes rapid neurogenesis can lead to defective cells. only 50% neurones end up becoming part of the brain and the rest are intentionally killed as part of the development process.
205
what processes refine the neural circuits?
apoptosis
synaptic pruning
206
what is myelination?
regional variation in the pattern of white matter pathways maturation
207
what is neuronal differentiation?
a process by which different subpopulations/types of neurones are generated. these subpopulations are specific to different parts of the brain, play different functions and use different neurotransmitters
208
what is axonal growth?
formation of an axon
209
what is adult neurogenesis?
generation of new neurones
210
how are neurones functional?
they differentiate, migrate, form connections and myelinated
211
what are the types of neurodegeneration?
"normal" age related decline
neuro traumatic diseases
neurodegenerative diseases
neuropsychiatric diseases
212
what are the consequences/mechanisms of neuroedegeneration?
death of neurones
fewer neurones take up less space -> smaller brain
loss of synaptic connections
axons degenerate
less "white matter"
smaller brains
213
what are the types of degeneration?
Fast
- stroke
- hypoxia
Slow
- neurodegenerative diseases
- normal age related decline
- repeated concussion
214
what are the general causes of neurone death/synapse loss?
hypoxia
excessive activity
idiopathic/sporadic
neuronal dysfunction, protein aggregations
monogenetic (Huntington's disease)
215
what is hypoxia?
lack of oxygen
cant generate enough energy
neurons die
strokes, transient ischaemic attack etc
216
describe excessive activity?
exciotoxic lesions in rodents
glutamate hypothesis in epilepsy
217
what is neuronal dysfunction, protein aggregations?
causes the neurone to undergo apoptosis
this apoptosis is not beneficial
compare to essential apoptosis in development
218
what is monogenetic (huntington's disease)
caused by mutation in a single gene
simpler than other degenerative disorders
mutation in the huntingtin gene
initial degeneration of neurones in the basal ganglia
219
what is the difference between neuronal death during development neurodegeneration?
apoptosis or programmed cell death enable elimination of defective or excessive cells characterised by cell shrinkage etc. necrosis enables eliminations of cells damaged by external physiochemical stress characterised by cell swelling and loss of membrane integrity
220
define alzheimer's disease
amyloid plaques
poor memory for recent events; other cognitive problems, emotional and personality changes, amyloid plaques and neurofibrillary tangles
221
define Parkinson's disease
lower dopamine in substantia nigra
motor tremors, stiffness and slow movement; disease progression is also associated with cognitive deficits, loss of dopaminergic neurones, neurodegeneration of other brain regions affecting other neurotransmitters
222
define huntington's disease
affected basal ganglia
uncontrolled movements associated with neurodegeneration in the basal ganglia, emotional and cognitive problems
223
what are the clinical characteristics of alzheimer's disease?
memory
initially, poor memory for recent events
more so than age related memory decline
other areas
- deficits in spatial navigation
- changes in ppersonality
- aggression/apathy
- depressive symptoms
224
name and describe the two main types of alzheimers?
sporadic/late onset
- no obvious cause or heritability
- most common
- apolipoprotein E (APOE)
early onset
- <10% oof cases
- 1-2% familial (inherited)
225
describe neurodegeneration in AD
initial areas of degeneration (temporal lobe)
general neuronal loss
neurofibrillary tangles
amyloid plaques
synaptic loss
- correlates with cognitive impairment
- particularly affects cholinergic and glutamatergic synapses
226
what are the two types of treatments for alzheimers?
drug and targeting pathology
227
how does drug treatment for alzheimers work?
initial aim of boosting cholinergic transmission
prolong presence of remaining ACh in the synapse
Acetylcholinesterase inhibitors
not very effective
nicotine patches
228
how does targeting pathology work for treating alzheimers?
divert APP away from amyloid
antibodies for amyloid
not very effective
229
what are the three main types of parkinsons disease?
idiopathic, drug induced and genetic
230
what is idiopathic parkinsons disease?
no identifiable cause
most common
231
what is drug induce parkinsons disease?
can be caused by antipsychotic medication
slightly different from parkinsons disesase
232
how rare is genetic parkinsons disease?
<5%
233
what are the clinical characteristics of parkinsons disease?
motor function and non-motor function
234
what is motor function?
tremors
rigid muscles
slowness or absence of movement
initially unilateral
very early symptoms in facial expressions
235
what is non-motor functions?
cognitive effects
emotional effects
not just a consequence of being aware of the movement problems
can characterise as a general slowing of brain function
236
what does degeneration in parkinsons disease look like?
degeneration is extensive before symptoms appear
80% neuron loss
would help to detect before such loss
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what are the treatments for parkinsons disease?
drugs, cell transplantation, deep brain stimulation, repair and recovery, possible in peripheral nervous system
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how does drug treatment work for parkinsons disease?
aim of replacing/increasing dopamine
but dopamine is rapidly metabolised
also does not cross the BBB
levodopa (L-DOPA)
dopamine agonists
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how does cell transplantation work for parkinsons disease?
aim of enhancing the function of remaining dopamine circuitry
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how does repair and recovery work for parkinsons disease?
possible in peripheral nervous system
cut finger nerve
axon regrows
connects to sensory cell or muscle
only if cell body remains intact
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why is CNS recovery not normal for parkinsons disease?
complexity of connection, as connections mature they change compared to those in the developing brain and are different to the stable connections in the PNS. also, would need to reconnect correctly which is possible in the spinal cord but almost impossible in the brain
