neurologic- dementia

Question 1

dementia=

Answer 1

decline in cognitive function (memory, judgement, emotions, listening, speech, reacting to the environment)
-loss of ordered neural function d/t several unrelated disorders

Question 2

alzheimers dementia?

Answer 2

65% of all dementia

-progresive and irreversible

Question 3

prevalence of AD occurs after

Answer 3

age 65

Question 4

65-75 percentage

Answer 4

10-15% have AD

Question 5

75-85 percentage

Answer 5

19%

Question 6

85 percentage

Answer 6

48%

Question 7

etiology of AD?

Answer 7

• aging
• idiopathic (90%): sporadic form generally appearing after age 65
• genetic (10%): familial form, onset less than 65 years

Question 8

cause of the genetic form of AD? (3 genetic components!!)

Answer 8

• APP gene (amyloid percursor protein) on chromosome 21 (those with down-syndrome will develop it much earlier in life)—> amyloid deposits indicate tissue damage
• PS1 on chr 14 and Ps2 on chr 1 (presenilin 1 and 2): code for proteins that form part of an enzyme, cleaves various proteins
• APoE (apoliproteinE) gene on chr 19- normally transports cholesterol, if mutated: gives rise to abnormal accumulation of proteins in brain

Question 9

two types of proteins in alzheimers?

Answer 9

Tau and AB

Question 10

pathology of AD? (4 main)

Answer 10

-CORTICAL ATROPHY: atrophy of cerebral cortex and loss of neurons, particularly in parietal and temporal lobes
-ridges formed by brain tissue (gyri) become slender
-spaces between these ridges (sulci) become more prominent
-loss of brain tissue= impeded transmission of signals throughout brain and loss of function
-NEURONAL LOSS in hippocampus and amygdala
(these are specialized area involved in cognition)
-SENSORY CORTEX MAINLY UNAFFECTED
-LOW LEVELS OF ACH

Question 11

hippocampus function

Answer 11

important part of memory, temporal lobe

Question 12

amygdala function

Answer 12

helps us to interact with our environment, temporal lobe

Question 13

microscopic lesions in AD: neuritic plaque

Answer 13

they are only detectable under microscope, usually found in autopsy
1) neuritic plaques: patches or flat areas composed of clusters of degenerating nerve terminals arranged around a central amyloid core. the amyloid core main component is amyloid beta, it is the rest of the breakdown of APP, which damages the cells, occurs OUTSIDE of the neuron

Question 14

microscopic lesions in AD: neurofibrillary tangles

Answer 14

2) neurofibrillary tangles: fibrous proteins wound around each other in a helical fashion, found in cytoplasm of cell WITHIN the neuron, tangles are resistant to chemical or enzymatic breakdown (exist even after necrosis of neuron)
- major component of the tangle= abnormally hyperphosphorylated form of protein Tau
- tau found within microtubules of cytoplasm

Question 15

In AD, the number and distribution of microscopic lesions…

Answer 15

contribute to intellectual deterioration—-> the plaques and tangles and associated neuronal loss affect the amygdala and hippocampus

Question 16

chemical changes in AD?

Answer 16

-decrease in choline acetyltransferase… enzyme that forms acetylcholine
so decrease Ach—> NT in cortex and hippocampus, associated w decreased memory

Question 17

manifestations of AD?

Answer 17

• occur decades after changes (subclinical progression of disease
• insidious onset, progression can be staged in terms of SEVERITY

Question 18

MILD AD manifestations (approx 2-4 years)

Answer 18

• individual usually not aware of changes but family and friends are
• loss of short-term memory (may repeatedly ask the same qs)
• careless work habits (occupation or hobbies)
• personality changes (more aggressive, careless)
• mild depression

Question 19

MODERATE AD manifestations (2-10 years)

Answer 19

• profound confusion “confusional state”
• depression
• becoming aware of own problems
• language problems–> paraphasias (speech disturbance resulting from brain damage, words are jumbled and sentences meaningless)
• neglected hygiene
• aggression—> enhanced by caregiver telling them what to do
• MOST cognitive loss occurs here

Question 20

SEVERE AD manifestations (~2years)

Answer 20

• severe mental impairment
• inability to respond to environment
• motor function issues
• sleep wake pattern altered
• minimal voluntary movement
• no self care
• rigid flexor posturing (clenched fists, shuffling walk)

Question 21

diagnosis for AD?

Answer 21

• no definitive test to diagnose AD: microlesions only seen under microscope
• may be made by exclusion (testing for other acauses of dementia)
• EEG, CT, MRI, electroencephalogram
• vitamin b12 defeciency (anemia?)
• STIs (HIV, syphilis- can cause dementia)
• thyroid function
• physician will always talk to family to compare pts actions to normal

Question 22

treatment for AD?

Answer 22

• NO CURE
• symptomatic management (depression, incontinence)
• GOAL= slow progression of disease
• behavioural and environmental manipulations

Question 23

pharmacology (Drugs) for AD?

Answer 23

1) gultamate receptor blocker= MEMANTINE
- stimulatory NT, a build up of glutamate is neurotoxic
2) ach-esterase inhibitors= ARICEPT
- this breaks down ach, so stopping it increases ach
- antidepressants (effexor)
- antipsychotics (resperidone)