Renske de Veer (rdeveer)
Summary Alzheimer’s disease and stress related disorders
Artikelen:
1. Golde, 2016 Overcoming translational barriers impeding development of Alzheimer’s
disease modifying therapies
2. Vernooij-Dassen, 2014 Raising the standard of applied dementia care research: addressing
the implementation error
3. Fotuhi, 2009 Changing perspectives regarding late-life dementia
HC 1: Personalized Dementia Care
Prevalence: 250.000 patients in the Netherlands (Age 70-75: 10%, Age 80-85: 20%)
An enlarged ventricular system is typically found in Alzheimer’s disease (AD). This type of change is
found with all degenerative diseases and is a non-specific finding reflecting the loss of brain tissue.
Some studies have pointed to temporal horn enlargements as most informative in AD, as it may
reflect the local damage to the medial temporal lobe. Recent studies suggest that knowledge of the
magnitude of the brain CSF (cerebrospinal fluid) volume is of interest in correcting for the dilution of
spinal fluid concentrations of proteins such as tau or hyperphosphorylated tau. These proteins are
experimentally used in diagnostic testing in AD.
- Alzheimer = amyloid, NOT vascular!
- Vascular dementia = vascular
Personalized dementia treatment & prevention
- Cardiovascular treatment (hypertension, cholesterol, diabetes)
- Lifestyle
o Diet, smoking, alcohol
▪ Nutrition: DASH-diet en mediterranean diet → bepaalde voedingspatroon,
beschermen tegen hart- en vaatziekten en dementie.
o Physical activity
o Preventing sedentary behaviour
o Sleep
- Care (day care, physical therapy, speech therapy, occupational therapy, home care, caregiver
support and education, casemanger).
AD risk genes → Amyloid pathway.
Strong interaction between different levels: cellular, organs, organisms, social scale.
Plaques and tangles → tussen de groep met en zonder dementia zit geen verschil. Hippocampus
atrophy verschilt wel van de groep.
Er is verschil tussen familaire Alzheimer (dominant overerfbaar) en Late Onset Alzheimer → moeten
anders behandeld worden.
Gehoorverlies en sociale interactie zijn gerelateerd aan cognitieve achteruit gang (dementia).
, Renske de Veer (rdeveer)
HC 2: Personalized & Translational Dementia Research & Care: Why we need something
completely different.
Why do we need change in Personalized & Translational Alzheimer research & care?
- No therapy has yet shown significant clinical disease modification. Overcoming translational
barriers can result in successful disease modification. (Trial failure; trials inadequate, largely
admitted)
- Pharma stops as result of failed trials.
- Better research proposals and trial designs are necessary that result in actually results, since
99.6% of more than 400 trials have failed and wasted 2-10 billion Euro’s.
- Prevention successes have been neglected
- Too reductionistic approach
- Better therapies (of 80% efficacy) are necessary to reduce Alzheimer cases.
- Hallmarks of AD are also observed in other diseases, thus knowing these hallmarks can
contribute to a better treatment for a range of diseases.
- Diabetes Type I Diabetes type II
- We forgot the complexity of LOAD
- Prevalence of Dementia is only increasing and has been expected to increase over the years.
How can we change Personalized & Translational Alzheimer research & care?
- Physical domain is related to B-amyloidose.
- Social domain is related to glycation.
Summary Alzheimer’s disease and stress related disorders
Artikelen:
1. Golde, 2016 Overcoming translational barriers impeding development of Alzheimer’s
disease modifying therapies
2. Vernooij-Dassen, 2014 Raising the standard of applied dementia care research: addressing
the implementation error
3. Fotuhi, 2009 Changing perspectives regarding late-life dementia
HC 1: Personalized Dementia Care
Prevalence: 250.000 patients in the Netherlands (Age 70-75: 10%, Age 80-85: 20%)
An enlarged ventricular system is typically found in Alzheimer’s disease (AD). This type of change is
found with all degenerative diseases and is a non-specific finding reflecting the loss of brain tissue.
Some studies have pointed to temporal horn enlargements as most informative in AD, as it may
reflect the local damage to the medial temporal lobe. Recent studies suggest that knowledge of the
magnitude of the brain CSF (cerebrospinal fluid) volume is of interest in correcting for the dilution of
spinal fluid concentrations of proteins such as tau or hyperphosphorylated tau. These proteins are
experimentally used in diagnostic testing in AD.
- Alzheimer = amyloid, NOT vascular!
- Vascular dementia = vascular
Personalized dementia treatment & prevention
- Cardiovascular treatment (hypertension, cholesterol, diabetes)
- Lifestyle
o Diet, smoking, alcohol
▪ Nutrition: DASH-diet en mediterranean diet → bepaalde voedingspatroon,
beschermen tegen hart- en vaatziekten en dementie.
o Physical activity
o Preventing sedentary behaviour
o Sleep
- Care (day care, physical therapy, speech therapy, occupational therapy, home care, caregiver
support and education, casemanger).
AD risk genes → Amyloid pathway.
Strong interaction between different levels: cellular, organs, organisms, social scale.
Plaques and tangles → tussen de groep met en zonder dementia zit geen verschil. Hippocampus
atrophy verschilt wel van de groep.
Er is verschil tussen familaire Alzheimer (dominant overerfbaar) en Late Onset Alzheimer → moeten
anders behandeld worden.
Gehoorverlies en sociale interactie zijn gerelateerd aan cognitieve achteruit gang (dementia).
, Renske de Veer (rdeveer)
HC 2: Personalized & Translational Dementia Research & Care: Why we need something
completely different.
Why do we need change in Personalized & Translational Alzheimer research & care?
- No therapy has yet shown significant clinical disease modification. Overcoming translational
barriers can result in successful disease modification. (Trial failure; trials inadequate, largely
admitted)
- Pharma stops as result of failed trials.
- Better research proposals and trial designs are necessary that result in actually results, since
99.6% of more than 400 trials have failed and wasted 2-10 billion Euro’s.
- Prevention successes have been neglected
- Too reductionistic approach
- Better therapies (of 80% efficacy) are necessary to reduce Alzheimer cases.
- Hallmarks of AD are also observed in other diseases, thus knowing these hallmarks can
contribute to a better treatment for a range of diseases.
- Diabetes Type I Diabetes type II
- We forgot the complexity of LOAD
- Prevalence of Dementia is only increasing and has been expected to increase over the years.
How can we change Personalized & Translational Alzheimer research & care?
- Physical domain is related to B-amyloidose.
- Social domain is related to glycation.
