This contains all the notes for the first part of the course Translational Neuroscience (MED-MIN16). It contains notes, images and remarks by the lecturers.
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MED-min16 Translational neuroscience
Summary Written exam I
Alzheimer’s Disease (AD)
Prevalence of AD: The older you get, the higher the chance is you’ll get the diagnosis of AD.
There is a difference between ‘pure’ Alzheimer’s and the mixed disease, meaning that the patient has
Alzheimer and vascular dementia, or another pathology (e.g. Lewy body).
Women have a higher estimate than men, because women get older.
The race also has an influence on getting AD, e.g. the lowest chance for Asians and Pacific islanders
and the highest chance for Hispanics. This might have to do with their life style.
Also, low-income countries have a bigger growth in numbers of people with dementia than high-
income countries.
Plaques → Amyloid depositions
Tangles → Tau aggregates
In a later stage, the tau-tangles occur.
The last stage will give the diagnosis (red circle).
Tangles are located inside a neuron, and plaques
are in between neurons.
Tau proteins keep the microtubules in place. In
AD they pair with other tau proteins and they
become tangled.
The order of affected regions:
1. Temporal lobe; memory and learning
2. Frontal lobe; thinking and planning
3. Parietal lobe; processing sensory information regarding the location of parts of the body and
interpreting visual information and processing language and mathematics.
For a diagnosis the CSF can also be used.
A lot of people form plaques and tangles, but only some get AD.
Important in AD: the hippocampus. This works like a file cabinet (looks like a sea horse).
Some AD patients don’t have plaques and tangles. Then the cause could be a mix of things.
E.g. Vascular dementia → microbleeds (amyloid angiopathy).
Aging brain: an accumulation of damage
e.g. See the brain as a box: during life there is damage. Some of this damage can be repaired and
some things can be compensated. There will be a point that the brain can’t compensate and/or
repair anymore. That’s when the problems start.
Mild cognitive impairment (MCI)
MCI can be a precursor of AD, but some people only get MCI and it doesn’t become AD. Some people
don’t even show their MCI, they are able to cover it up.
Cognitive functions are: attention, memory, speed, executive function and language.
1
,A MCI patient has more problems than with normal aging. There are no big problems in daily life, but
you can see the problems in cognitive functions. It has an influence on 2 or more cognitive domains.
There are more people with MCI than we know of. This stage is also less well-known, because the
symptoms aren’t that severe as AD.
Diagnosis:
A general practitioner (GP) (=huisarts) can give a diagnosis due to tests and talking to the patient and
relatives. If the GP can’t diagnose it, the patient is send to a geriatric practitioner.
There is a focus on different parts of cognitive function:
- Memory (episodic; what happened?) (Semantic; the capital of France is..?)
- Language
- Orientation
- Problem solving
- Mental speed and flexibility
- Visual perception (visuo-construction and (facial) recognition)
An example of a cognitive test is the clock test. The more severe the cognitive impairment is, the
harder it is to draw a clock with a specific time.
Other symptoms:
- 50-70% of dementia is AD
- Slow process
- Cognitive problems
- Problems/changes in daily living
o Coordination
o Dress up
o Character changes
o Sequence of tasks
o Aggression
o Apathy
o Loss of interest
o Depression
In AD there’s a big difference between genetic and non-genetic.
Non-genetic could be:
- ‘life-long’ stressors (tobacco, alcohol, inactivity, diet, stress, sleep)
- Disease burden
- Coincidence (“bad luck)
Most of the drug trials don’t have a positive effect. Now the focus is on prevention, there’s focus on
lifestyle (exercise, diet, medication, blood
pressure, social activities, mood).
→ improving physical health
→ improving cognitive reserve
→ improving quality of life
Summary:
1. Not one single cause for AD
2. Not one single therapy
3. Prevention focus on lifestyle
2
, There’s not 1 study giving perfect results, it’s a combination.
People who are involved:
- Person with AD
- Informal caregiver: partner/child
- Formal care diagnosis: GP/geriatrician/neuropshycologist
- Formal care after diagnosis: occupational therapist/GP
- Scientific researcher
An early diagnosis can be either positive and/or negative.
Negative: If you are early diagnosed, but don’t have big symptoms yet, it can scare you a lot and
make you depressive as well.
Positive: You can prepare yourself and relatives for what is coming and start a possible treatment
earlier.
Use of biomarkers for diagnosis: PET, MRI, CSF and blood.
There are both advantages and disadvantages on the use of biomarkers.
Disadvantage: The levels of AB could be elevated, but that doesn’t mean that the patient has AD.
Scaring people with results that might not become true.
Advantage: Preparing people on living with AD. Knowing it early, then treatment could be started
earlier as well.
History
Victor of Aveyron: first child described with ASD.
Leo Kanner first described ASD as a genetic disorder.
Bruno Bettelheim said that ASD was caused by very
distant mothers.
Hypothesis 2: In the 70’s they did twin studies where
they found that ASD is a combination of genetics and
environmental factors.
People created a fear of vaccines, because they said it caused ASD: this is not true.
It’s important to know the difference between a hazard and a risk.
Hazard = potential thing to happen
Risk = a probability that it will happen
What doesn’t help with the fear of vaccines: asymmetrical updating. If you are anti-vaccines, your
computer will automatically find more about this, because of algorithms.
Epidemiology
The prevalence for ASD is 1/58.
The prevalence increases over time. Proposed explanations for this are:
- Awareness
- Better identification
3
, - Sensitive diagnostic tools
- Broader classification systems
- Environmental factors
- Diagnostic substitution: Doctors place e.g. mental retardation under ASD, for patients to get
financial help from the government.
- Media
Gender bias:
Females are more protected to ASD. They need a higher mutation load to have ASD. They have a high
prevalence of X-linked candidate genes for ASD.
Males are less protected. An increased exposure to testosterone during pregnancy leads to an
increased risk of ASD.
Hormonal imbalance: the reduced expression of the RORA gene in ASD brains leads to a reduced
expression of aromatase, which leads to an increased level of testosterone.
If you have more testosterone in the brain, you have more chance on ASD.
The extreme male brain hypothesis can be tested with the hand:
If your index finger is longer than your ringer finger, then you are more exposed to testosterone
during pregnancy. The hypothesis states that then there is higher chance to have ASD.
The social brain
A patient doesn’t pick up any emotions from looking at the movie where the triangles and circle
interact. This is what is meant by a social brain; a healthy subject gives emotions to the figures.
Oxytocin is involved from the prenatal stage to death: it slowly becomes the molecule with makes
you socialize, fall in love, orgasm. It’s a lifelong molecule.
Vasopressin can be compared with oxytocin; it’s a hormone and neurotransmitter.
DSM5 criteria
We now only use autism spectrum disorder, where earlier it were all different diagnosis (PDD-NOS,
autistic disorder, Retts, Asperger’s).
ASD can be divided in two different groups:
Persistent deficits in social communication and social Restricted, repetitive patterns of behavior, interests, or
interaction activities, as manifested by at least two of the following,
currently or by history
1. Deficits in social-emotional reciprocity 1. Stereotyped or repetitive motor movements, use of
- Abnormal social approach objects, or speech
- Failure of normal back and forth conversation - simple motor stereotypies
- Reduced sharing of interests, emotions or affect - lining up toys or flipping objects
- Failure to initiate or respond to social interactions - echolalia = repetition of verbal behavior
- echopraxia = mimicking behavior
- idiosyncratic (strange) phrases
2. Deficits in nonverbal communicate behaviors used for 2. Insistence on sameness, inflexible adherence to routines, or
social interaction ritualized patterns of verbal or nonverbal behavior
- Poorly integrated verbal and nonverbal - Extreme distress at small changes
communication - Difficulty with transitions
- Abnormalities in eye contact and body-language - Rigid thinking patterns (very fixated interests)
- Deficits in understanding and use of gestures - Greeting ritual
- Total lack of facial expression and nonverbal - Need to take same route or eat same food everyday
communication
4
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