Alzheimers Flashcards
What are plaques?
- beta amyloid plaques are made from chemically sticky monomers that bind together just outside neuron cell B
- they can get between neurons which disrupts signalling between them (impaired brain function)
- they can start immune response (inflammation) which damages surrounding neurons
What is amyloid angiopathy?
- when amyloid plaques deposit in blood vessels
- weakens walls
- increased risk of haemorrhage/rupture
What is APP and what does it do?
- amyloid precursor protein
- helps neuron reproduce and grow
- usually gets shopped up to make soluble peptide
Which monomers form beta amyloid plaques?
- amyloid beta monomers
- these fragments are made when beta secretase and gamma secretase pair up
What are neurofibrrillary tangles?
- when the TAV protein changes shape and stops supporting the microtubules in the neuron
- TAV clumps together
What is the result of neurofibrillary tangles?
- non functioning microtubules can’t signal as well
- results in apoptosis
What happens in the brain as neurons age?
- gyri (ridges) get narrow
- sulci (grooves between gyri) get wider
- when atrophying (shrinking) ventricles (fluid filled cavities) get larger
What is Alzheimer’s disease?
- irreversible/progressive brain disease that destroys memory and thinking
- marked atrophy of cerebral cortex and loss of cortical and subcortical neurons
What does Alzheimer’s impact?
- intelligence
- judgment and behaviour
- memory
- language
What are the 4 genes that influence gene development?
• APP - fault on chromosome 21
• presenlin 1 and 2 - faults on chromosome 1 and 14
• apoliprotein E (of which three forms - APOE2,3,4)
Which genes influence young people and which the elderly?
- APP and presenlin 1 and 2 affect young people
- APOE affects over 65s
What are the essential jobs of neurons?
- communicate with eachother
- carry out metabolism
- repair themselves
Alzheimer’s disrupts all three!
What are the clinical features of Alzheimer’s?
- memory loss
- language decline
- apraxia
- agnosia
- progressive loss of executive functions
- behavioural changes
- loss of sight (relative/complete)
- depression
What is apraxia?
Inability to carry out skill/motor activity
What is agnosia?
Failure to recognise objects, places and people
What is the progression of Alzheimer’s?
MILD - memory loss, confusion, anxiety, poor judgement
MODERATE - problem recognising people, wandering, agitation
SEVERE - extreme brain shrinkage, completely dependent, increased sleeping, weight loss
How is Alzheimer’s diagnosed?
- med hx and sx
- physical exam (inc neurological)
- mental state evaluation (check memory and attention span)
- blood/genetic test (for APOEe4 gene)
- imaging (CT, MRI, PET)
- magnetic resonance imaging
What is preventative care for Alzheimer’s?
- eating healthy and exercising
- eating fatty, cold water fish (tuna salmon)
- antioxidants, vit a e c (help prevent damage caused by free radicals)
- maintains normal BP
- keeping mentally and socially active
What is the mini mental state examination?
Measures cognition
- assess orientation, registration, recall, language and attention
- uses 30 point scale
- 5-10mins to complete
- minimal training required
- if untreated, disease deteriorates 3 points annually typically
Lifestyle changes for Alzheimer’s?
- regular walks
- bright light therapy
- calming music
- pets
- relaxation training
- ID bracelets
How is Alzheimer’s treated?
- mild with donepezil, galantamine
- severe with memantine
