Complete summary of cases, lectures and journal clubs of the minor course BBS3022 ''Clinical and personalized nutrition''. This course is the seconds course of the nutrition minor. Following BBS3021 (The role of nutrition in the life cycle in relation to global health).
BBS3022 Clinical and Personalised Nutrition - Art Muijsenberg & Camil Gastreich
BBS3022 Clinical and Personalised
Nutrition
Academic year 2018-2019
ART MUIJSENBERG, CAMIL GASTREICH - MAASTRICHT UNIVERSITY - FACULTY OF MEDICINE, HEALTH AND LIFE SCIENCES
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, BBS3022 Clinical and Personalised Nutrition - Art Muijsenberg & Camil Gastreich
BBS3022 Clinical and Personalised Nutrition
Theme 3: Nutrition and chronic disease development 3
Case 11: Alzheimer's disease 3
Case 12: ‘’What’s good for your heart is good for your brain’’ 14
Theme 4: Clinical nutrition 33
Case 13: If the gut works, use it, but else….. 33
Part 1 33
Part 2 42
Lecture: Parenteral nutrition 48
Case 14: It is all about ERAS 52
Case 15: When the liver does not appreciate infused nutrition 62
Theme 5: Personalised nutrition 70
Case 16: A personalized diet for extreme situations 70
Lecture: personalized nutrition 81
Case 17: It is time to get personal 83
Journal Clubs 97
Journal Club 4: Dietary prevention of neurodegenerative decline 97
Journal Club 5: Should we panic because of PEPaNIC 101
Journal Club 6: Predicting personalized responses to nutrition 105
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, BBS3022 Clinical and Personalised Nutrition - Art Muijsenberg & Camil Gastreich
Theme 3: Nutrition and chronic disease development
Case 11: Alzheimer's disease
WHAT IS DEMENTIA?
Alzheimer • Amyloid B plaques
More prevalent in women • Tau
Develops in stages Diet (insulin resistance)
Cognitive reserve Drugs?
Change in brain structure (atrophy) Symptoms (short-term) memory loss
Age dependent Cognitive decline
Markers
1. Normal neurocognitive function (neurobiology of learning and (different types of)
memory)?
1. Long term potentiation and long term depression
2. What is dementia (different forms)?
1. Alzheimer's disease (different stages of the disease)
2. Prevalence of dementia and alzheimer's disease
3. What is the aetiology of alzheimer's disease?
4. What are the risk factors for alzheimer's disease (e.g. age, diet)?
5. What are the symptoms of alzheimer's disease?
6. How is Alzheimer's disease diagnosed?
7. How can Alzheimer's disease be treated/prevented (e.g. by nutrition)?
1. Normal neurocognitive function (neurobiology of learning and (different types
of) memory)?
50% of a persons cognitive function at old age is determined by childhood intelligence, which has
an important genetic component.
Different types of memory
Sensory memory: Automatic response within a
second
Short-term memory: recall of several seconds to a
minute (limited capacity) without rehearsal.
Long-term memory: More information and
Declarative: facts, explicit conscience effort.
Non-declarative: skills and practice (implicit
memory, results from experience).
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, BBS3022 Clinical and Personalised Nutrition - Art Muijsenberg & Camil Gastreich
Long term potentiation and long term depression
Synaptic plasticity involves several processes by which the brain undergoes neural changes.
Plasticity is usually dependent on glutamatergic synapses. Through these changes the efficacy of a
particular synapse can increase or decrease depending on the particular change. The efficacy of a
synapse can be changed by increasing or decreasing the amount of neurotransmitter presynaptically
released across the synapse or by increasing or decreasing the amount of AMPA receptors present
postsynaptically (thereby making that synapse
more sensitive). Furthermore, the changes which
occur at one synapse effects the entire network
of neurons to which that synapse is connected.
Two of these mechanisms which commonly
affect the way efficacy of a synapse are Long
Term Potentiation (LTP) and Long Term
Depression (LTD).
Brain plasticity: ongoing process of forming new synapses and breaking up old ones.
Long Term Potentiation
This diagram outlines the mechanism of LTP. In LTP the AMPA receptors become sufficiently
excited which leads to an influx of Na+ which leads to a dramatic depolarisation of the postsynaptic
cell (Excitatory Post Synaptic Potential; EPSP). This EPSP releases the Magnesium ion blocking
the NMDA receptor, and allows a Calcium-glutamate molecule to enter the cell. As intracellular
[Ca] increases protein kinases such as calcium/calmodulin-dependent protein kinase II (CaMKII)
and protein kinase C (PKC) are activated. The activation of these two proteins allows for the 2
major mechanisms of LTP to proceed. These two mechanism are the phosphorylation of existing
AMPA receptors (AMPAr's) thereby increasing their sensitivity, and the increase of postsynaptic
AMPAr's due to kinase activity. In the late phase of LTP the synaptic changes that began in the early
phase are continued, and are dependent on gene expression and protein synthesis. Late phase LTP is
induced when sustained activation of the early phase kinases (CaMKII and PKC) activate the
extracellular signal-regulated kinase (ERK). These kinases phosphorylate signal and nuclear
proteins which in turn lead to protein synthesis, morphological changes of the neuron, and gene
expression. Late phase LTP changes include both postsynaptic changes as well as presynaptic
changes due to retrograde signalling. Postsynaptic changes include increased dendritic area and
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