Dementia/PD + role of nutrition 2 Flashcards

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1
Q

What is the total % of modifiable risk factors in dementia?

A

40%

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2
Q

What are the most potential nutrients (prevention dementia)?
And food groups?

A

B vitamins: B6, B12, Folate
Antioxidants: E, flavonoids
Vit D
MAcronutrients: omega-3-FA

Alcohol: dose & type
Coffee & tea
Fish + seafood
Veg + fruits (gr leafy + berries)

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3
Q

Mind diet combines the ….. and ….. diets

A

DASH
Mediterranean

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4
Q

MIND diet adherence: better cognition + larger brain volume

A

ok

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5
Q

multidomain interventions have..

A

▪ At least 2 combined interventions in 1 study

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6
Q

FINGER trial: what is it?

A

Finland, 2 years, group with CVD risk: social activity, physical exercise, vascular + metabolic monitoring, active diet, cognitive training.

+25% overall cognition

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7
Q

FINGER now also in NL. Ongoing. What lifestyle interventions are people undergoing?

A

Dietary counseling (mind + vit D)
Fortasyn connect (muliti-nutrient drink)
Physical exercise
Cognitive training
Sleep counselling
Stress management
Vascular risk management
Social acitivies

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8
Q

What is the fortasyn connect drink (souvenaid) supplied with?

A
  • Supplied with precursors for neurotransmitters, such as choline, Vit B, phospholipids, DHA (=omega-3)
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9
Q

What are the two most important omega-3-FA?

A

DHA and EPA

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10
Q

What is the mechanism of action of DHA and EPA?

A
  • brain cell membranes
  • inflammation
  • oxidative stress
  • vascular factors
  • cerebral blood flow
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11
Q
  • Seafood consumption (1 or more/week): significantly correlated with less AD pathology
     Only among APOE4 carriers
  • Seafood consumption not correlated with brain infarcts or with Lewy bodies
  • Seafood consumption correlated with higher brain levels of mercury
     Higher mercury levels not correlated with increased brain neuropathology
A

ok

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12
Q

Why would a ketogenic diet help in neurodegenerative disease?

A

They are characterized by a detoriation of glucose metabolism. Increase ketone availability: proposed protective mechanism

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13
Q

What are aspects to consider in human gut-brain studies?

A

causality
Small sample size
Corrections for multiple testing lacking
Adjustments for confounding: diet

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14
Q

What are Methodological challenges in nutr/ brain studies?

A
  • Method of nutritional status assessment is difficult (memory, FFQ have fixed list of nutrients)
  • Timing of assessment: changes visible after years (duration of follow-up)
  • Confounding of non-dietary factors
  • Sample selection
  • Multidimensionality of diet
  • Multidimensionality of underlying mechanisms
  • Multidimensionality of cognitive function
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15
Q

How long does it take before parkinson’s symptoms occur when the substantia nigra starts to be degraded?

A

20 yrs after degradation

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16
Q

Signs of PD?

A
  • Slowness
  • Rigidity (range of motion decreased)
  • Tremor
  • Postural abnormalities
17
Q

Not only in the brain, but also peripherally (heart, gut): PD gives rise to many non-motor symptoms. Recall them

A
  • sleep
  • autonomous (urinary problems, hypotension)
  • GI (swalling, delayed gastric emptying, constipation)
  • sensory
18
Q

Which is more predictive of QoL (quality of life) in PD: motor or non-motor symptoms?

A

non-motor

19
Q

Pathophysiology
- Abnormal deposition of alpha-synuclein (lewy bodies) -> spectated to be the cause
- Neuronal loss in the substantia nigra
- Loss of dopamine in the striatum
- First motor symptoms appear after loss of 50-70% of substantia nigra (nigral projection)

A

ok

20
Q

What is the theory of alpha-synuclein spread as a prion?

A
  1. Defected neuron with pathological alpha synuclein
  2. Excrete pathological alpha-nsynuclein
  3. Infects healthy neurons
  4. Alpha-syn in healthy neuron: abnormal configuration and become pathological
21
Q

What are problems in treating PD?

A
  • not one single disease entitiy, but syndrome
  • treating one mechanism doomed to fail
22
Q

What may contribute to increase of PD?

A

 Pesticides may contribute to increase of PD