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on 29 October 2013

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Transcript of Dementia

Dementia: Focusing on Alzheimer's
By: Christopher Greenwald
PharmD. Candidate
Class of 2014

Dementia Brief History
"A woman in her early 50s was admitted to a hospital because of increasingly odd behavior. Her family reported that she had been showing memory problems and strong feelings of jealousy. She also had become disoriented at home and was hiding objects. During a doctor's examination, the woman was unable to remember her husband's name, the year, or how long she had been at the hospital. She could read but did not seem to understand what she read, and she stressed the words in an unusual way. She sometimes became agitated and seemed to have hallucinations and irrational fears."
Dementia Brief History
Description of Auguste D. in her early 50's
First scientific documentation of the disease by the German doctor Alois Alzheimer
After she died in 1906, autopsy revealed that her brain appeared shrunken, clumps of proteins called plaques, neurofibrillary tangles, and arteriosclerotic changes.
"Senile Dementia" was the currently used terminology for dementia at this time
Latin for "old age" "deprived of mind"
What is dementia?
Memory loss that gets worse
Chronic deterioration of cognitive function
Interference in social and occupational functioning
Trouble using understanding words
Getting lost in well known places
Most common cause of dementia
Degenerative disease
Multiple contributing factors including genetic and environmental influences
Second most common
Cerebral infarct most common cause
Coexist with Alzheimer's
May be a history of stroke, transient ischemic attacks, vascular disease, and associated cerebrovascular risk factors such as hypertension or hyperlipidemia
60%, 5 year mortality rate due to complications
APP(Amyloid Precursor Proteins) produce Beta-Amyloid polypeptides which are hypothesized to be involved in neuronal function and perhaps cerebral development
It is thought that a gene mutation to the APP altered production in the beta amyloid polypeptides thus causing the plaques.
Pathophysiology (Cont)
Neurofibrillary tangles
Tau is protein responsible for the growth and development of the axon
Excessively phosphorylated tau protein
Pathophysiology (Cont)
Loss of cholinergic neurons
Decreased acetylcholine
(MMSE) Mini-mental state exam
How to interpret MMSE scores?
30 for none
26-29 questionable
21-25 mild
11-20 moderate
0-10 severe dementia.
Nonpharmacologic Treatment
Aim to diagnose the cause of the dementia.
Treat any reversible cause appropriately
Treat neurologic manifestations of the dementia including cognitive dysfunction and behavioral problems with appropriate pharmacological and non-pharmacological means
Educate family and patient on diagnosis, prognosis, treatment options, anticipated care issues, and complications
Pharmacologic Treatment
Cholinesterase Inhibitors
Donepzil (Aricept) -Mild-Severe
ADE- GI, nausea, vomiting diarrhea
Rivastigmine (Exelon) -Mild-moderate
ADE- GI, same as above
Galantamine (Razadyne) -Mild-moderate
ADE- GI, same as above
Donepezil (Aricept)- Mild-severe
ADE- GI, nausea, vomiting, and diarrhea
Rivastigmine (Exelon)- Mild-moderate
ADE- GI, same as above
Galantamine (Razadyne)- Mild- moderate
ADE- GI, same as above
Pharmacologic Treatment
NMDA Antagonist
Memantine (Namenda) Mild- Severe
ADE- Confusion, headache, and dizziness
Identify symptom and causative factor
Eliminate trigger
Eg. background noise, glare, television, etc.
Accommodate the patient
Things to avoid
Anticholinergic drugs

Over 100 years since the discovery of Alzheimer's
Current therapies will delay disease onset
Accommodate patient and caregiver needs
Be compassionate
The Future
(Tasigna) nilotinib
Used for CML (chronic myelogenous leukemia)
Appears to eliminate abnormal protein buildup in the brain
Reported to target the alpha-Synuclein and tau proteins

Pharmacologic Treatment
Cholinesterase Inhibitors (MOA)
Inhibit acetylcholinesterase, to increase concentration of acetylcholine.
Pharmacologic Treatment
NMDA Antagonist (MOA)
Antagonist at the NMDA receptor, thus blocking glutamine and glycine from binding to receptor to inhibit cation channels (Ca++, K+)
Full transcript