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NEURODEGENERATION - FP
Terms in this set (21)
most common form of dimentia
... are associated with alzheimer's
why are they bad?
Extracellular Neuritic plaques
Intracellular Neurofibrillary tangles
Intracellular Phosphorylated tau
AND THE BRAIN DONT GET RID OF THEM!
they are such burden for the neurons and resulting in oxidative damage and death of neuron
Places where A8 plaques are?
_____is prominently impaired in early AD
temporal lobe and hipocampus
important for memory
medial temporal lobe, is prominently impaired in early AD
where and what does tau do
it surrounds axons and dendrites and inhibit electrical transmission
In Rotterdam study, average age of dementia diagnosis is ____yo and symptoms beings ____ years before the diagnosis.
Life expectancy after diagnosis is __ to __ years
3 to 11
Acquired risk factor for Alzheimer's
Hypertension, Dyslipidemia, Altered glucose metabolism
unmodifiable risk factors for alzheimer's
Mutation in amyloid precursor (APP) OR IN psen1, 2
hypertension lead to dementia?
--> arterial stiffness and BP variability --> impaired blood flow to the brain
observational study suggest that treatment of hypertension reduces risk of dementia but clinical trials cant say the same
difficulty to perform learned motor skills.
usually occur AFTER deficits in memory and language become apparent
Seizures in AD patients is usually subclinical
EEG - brain wave activity
Molecular biomarkers for A-b protein deposition (Alzheimer's)
Low cerebrospinal fluid (CSF) Aβ42 (or Aβ42:Aβ40 ratio)
Positive amyloid PET imaging
Biomarkers of tau deposition (a key component of neurofibrillary tangles) include:
- Increased CSF total tau and phospho-tau
- Evidence of cerebral tau using a tau-specific PET tracer (in development) 
Alzheimer's disease is characterised by
1. inability to function at work/daily activity
2. a decline in previous performance
3. CAN NOT explained by delirium or major psychiatric disorder
4. cognitive impaiment is established by history taking
5. cognitive impairment involves a minimum of 2 of the following
- impaired ability to acquire new information
- impaired reasoning, judment and handling complex tasks
- impaired visuospatial abilities
- impaired language function
- changes in personality, behaviour
Treatment - Cholinesterase inhibitors
how and why does this work?
Work by increasing cholinergic transmission by inhibiting cholinesterase at the synaptic cleft.
AD patients have reduced cerebral content of choline acetyl transferase leading to a decrease in ACH synthesis and impaired cortical cholinergic function
Treatment - Memantine
it is a NMDA receptor agonist, it blocks the binding of glutamate to this receptor and believed to be neuroprotective (reduce damage and improve symtioms)
EFFECTIVE BUT NOT OPTIMAL
Glutamate is the principal excitatory AA neurotransmitter, excessive binding of glutamate to NMDA receptor leads to ROS - which happens in AD
also may be induced by ischaemia
Nutrition of AD patients
inadequate nutrition is common and associated with increased morbidity and mortality!
High calorie diet/oral supplements can be helpful
Assisted feeding tpp
The aim of cognitive rehabilitation
to help patients in early stages of dementia to maintain memory and higher cognitive function
Estrogen replacement and anti-inflamatory drug for AD treatment
Estrogen replacement - no evidence that its beneficial
Antiinflam drug - on going investigation. has to be very specific
how about ginko biloba, omega3-FA, statins and vitamin B?
safe but no evidence to be beneficial, at least not in a long run
high cholesterol is one of the risk factors for AD, why is statins not beneficial then?
because neurons have already DIED! by the time the patients receive the treatment
Difference on active and passive vaccination against amyloid beta
o Give the patient amyloid beta for the APC to recognise and present it to T cell. Result: B cells secretes Anti-Abeta antibodies
o Give the antibody (protein with a target antigen - amyloid beta) to trigger normal immune respons to clear the amyloid beta
How does active vaccine, AADvac1, against pathological tau proteins works?
The vaccine works by triggering the immune system to remove tau AND shift microglia phenotype from pathologic to protective
- only up to animal study but then was shown unhelpful
THIS SET IS OFTEN IN FOLDERS WITH...
Neurophysiology 1 - FP B.bmed
Enteric nervous system - FP B.bmed
Gut-Brain axis - FP - B.bmed
Multiple Sclerosis - FP B.bmed
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