Beth-dementia

Question 1

Intro to Alzheimer’s

Answer 1

It is a from of dementia, loss of brain cells with shrinkage of the brain, gets more and more. Lasts 3-20 years avg 7-8, no cure, around 60% of dementia cases. Risk increases after 65, ppl living longer, overtook cardiovascular disease as leading cause of death, 42% have family or friend AD, annual cost is a lot

Question 2

What are some other forms of dementia

Answer 2

Vascular, focal dementias including posterior cortical atrophy, semantic dementia , parkinsons and huntingtons

Question 3

Symptoms of AD

Answer 3

1. Mild dementia: memory loss (episodic and semantic) impaired thinking and decision making but still independent 2. Moderate: confusion, disorientation, apathy, personality changes (withdrawn, paranoid, neglect), sundowning, hallucinations 3. Severe: forget self, don’t recognise anyone, loss of mobility and bodily functions

Question 4

Assessment for Ad

Answer 4

Mini mental state exam: repeat and recall object names, the date, where are you, name common object, following 3 step instructions, writing grammatical sentence
Copying an image of intersecting pentagons- as can’t compute complex visual motor mappings

Question 5

AD effects on the brain

Answer 5

Reduced levels of glucose and NTs (ach. Dopamine, glutamate). Pet uses radioactive G to measure metabolism. Beta amyloid plaques- fragments of beta amyloid protein released from neurone membrane and clump, become insoluble and interfere. Neurofibrillary tangles: neurones have microtubules and transport materials held by tau (protein), tau becomes separated causing Microtub to disintegrate, tau forms tangles which stop transport, cell death. Plaques AD spec, tau depositions in others-causes neuronal loss:brain shrinks and gaps expand

Question 6

History of AD

Answer 6

Alzheimer German psychiatrist studied changes post-mortem, August (patient) admitted for loss of memory, disorientated, hallucinations, incontinent- examined piece dead and found nuerofibrillary tangles and plaques. In 1910-60 called senile dementia in elderly and pre senile in younger but 60s onwards, realised the same. In 80s, plaques and tau id, in 90s, genetic risks from genome, 2000 used neuroimahine and 2010 brain connectivity

Question 7

AD and default mode network

Answer 7

Abnormal associated w memory retrieval, emyloid deposition may explain memory problems early on. May spread within functional networks, dmn at greater risk at greater metabolic rate

Question 8

Genetic risks to AD -familial AD

Answer 8

Form called familial AD, rare but common for early onset, clear genetic basis. AD is an autosomal recessive disease but familial AD is autosomal dominant, on 3 diff chromies, presenilin 1 on 14, 2 on 1 and amyloid beta precursor protein on 21-each causes plaques. Can use genetic testing

Question 9

Late onset AD genetic risks

Answer 9

Having other family W disease increases prob but only small. Gene APOE on 19 has 3 alleles, one copy of allele 4 increases risk by 4 times, 2 copies by 10-20 times but some don’t develop the disease

Question 10

Environmental risk factors for dementia

Answer 10

Saturated fats, red meat increase, med diet decrease. Gu 2010 analysed diets of 65 years old and 4 years alter. Those without dementia had med diet, moderate alc and smoking increased risk in apoe4 carriers. Bad gut microbes trigger inflammatory response, releases cytokines that cross blood brain barrier and damage cells

Question 11

Diagnosis

Answer 11

Happens slowly, starts with mild cog impairment: forgetting appointments and recent events, train of thought, misplacing. Need increasing deficits in at least 2 areas of function and severe problems that interfere W daily life. Mci when deficits milder, early, could be due to depression, heave to repeat every 6motnhs to id. Only 12% with mci over 65 have dementia after 1 year, after 5 it’s 50%

Question 12

Mci and brain images

Answer 12

Whitwell: degeneration of hippocampus in mci patients 3 years before diagnosis, brain vol diffs (reduced in temp and anterior lobes). Mci important as new treatments effective at this point. Chandler 2019: wellness training shows biggest effect on qual of life (habit training, writing things down) brain games less effective

Question 13

Cognitive reserve

Answer 13

High levels of intelligence and education allows ppl to function normally in early stages. The nun study Kemper 2001: nuns did annual assessment of physical and cog function and donated brains. Also analysed thier autobiographies and found those W dementia had lower scores in early autobiographies. Nuns W college degree lived longer and more mentally healthy. Eclipse study brain study- no effect of years of education but more educated ps less likely to be diagnosed

Question 14

Treatments for dementia -therapies and vitamin D

Answer 14

Brain training, better nutrition, reminiscence therapy (promote interactions). Ppl W alcoholism have vit b1 deficiency as poor absorption which causes brain damage and wernicke korsakoff syndrome (like dementia). Those W mci found 30% less atrophy in fit b group (small sample, only mci, atrophy may not be related).

Question 15

Treatments for dementia- AcH, inhibitors and recent trials

Answer 15

Cholinesterase inhibitors boost AcH by inhibiting enzyme that breaks it down, half AD ps showed benefits for milder AD. For more moderate: nmda inhibitors block glutamate as it’s released in large amounts and becomes toxic. But don’t stop progression, only work for some, spenny, only prescribed in moderate ps. 2022 trial with early ad had anti amyloid antibody infusions -reduced amyloid plaques supports amyloid hyp, showed improved cognition

Question 16

Executive control definition, where atrophy isn’t found, hippocampus functions

Answer 16

EC: maintaining a continuous task while ignoring irrelevant info/doing two things at same time. Atrophy doesn’t affect moving or seeing. Hippo used for memory and navigation - atrophy here linked to lack of episodic , found in temp, one in each hemi

Question 17

Memory in AD badely and backman

Answer 17

Badely- deficit in recall and recognition, damage to memory traces not just retrieval . Backman: 3-6 years before diagnosis, AD had lower mean memory perform, little chnage over time , recognition and recall similarly impaired but free recall harder in both groups

Question 18

Biology and mci

Answer 18

Whitwell- shrinkage before diagnosis leads to mci, atrophy at worst in hippocampus. Hippo deep in medial temp lobe. Atrophy affects temp, anterior, inferior and medial regions of temp

Question 19

Semantic memory and language

Answer 19

Left hemi has language and processing, anterior and inferior front lobe understands and creates words, atrophy causes semantic and language deficits. AD causes vocab shrinkage, greater loss for harder words as used less and learned later. Impaired object naming correlated W loss of cortex in L anterior temp lobe.

Question 20

Examples of semantic tasks and physiological methods

Answer 20

Showing how an object is uses, names of objects, faces, categories NOT numbers as magnitude in diff place in brain. TMS: transcranial magnetic stimulation, can be used to inhibit temporal lobes to disrupt semantic tasks

Question 21

Cog processes in executive control

Answer 21

Frontal lobes important, AD have trouble concentrating, making decisions, planning complex actions, coordinating activity. Badely: digit span task, repeat digits and motor tracking task by holding stylus on spinning point, can increase diff to find baseline. When asked to do both at same time, AD more impaired than controls

Question 22

AD and personality changes

Answer 22

Behavioural symptoms like irritability, agitation, outburst, repetitive behaviours. Linked to lack of cog control and frontal lobe atrophy. Atrophy of orbitofrontal cortex leas to apathy as reward value in the frontal pole

Question 23

Sensory functions

Answer 23

Later AD still has seeing hearing and moving but without knowing what they see/hear or where they are going. Primary sensory and motor areas are unaffected. Can lead to hallucinations, talk to tv, scared of shadow or holes in the floor

Question 24

Case of iris murdoch -garrard et al

Answer 24

Born in Dublin 1919 studies in Oxford and Cambridge, became a writer. Married john bayley who wrote book on thier life, show how high iq did not stop AD. mini mental state exam: rapid decline with poor recognition, naming and spelling in her own book (20/30-10/30 in a year). Worst atrophy in temp, par, hipp lobes. In cookie theft test- had test anomia (can’t find word). 3 novels analysis under the net, the sea, the sea and Jackson’s dilemma. Reduced vocab in book 3, more basic words, shorter phrase length

Question 25

Other types of dementia

Answer 25

Strokes can cause dementia: in descending prevalence: AD, vascular dementia, mixed (ad and vasc, Lewy body, frontotemporal, Parkinson’s and other

Question 26

Vascular dementia causes

Answer 26

Most common in Asia, loss of function due to reduced blood supply to the brain e.g. from stroke caused by blocked artery (blood clot/thrombosis) or bleed due to burst artery (haemorrhage). Deprives brain of 02 and nutrients so cells die causing lesion/infarct, each small stroke causes further deterioration as increases chance of another. Many have hypertension, smoking, diabetes and high cholesterol.

Question 27

Vascular dementia symptoms

Answer 27

Symptoms appear suddenly after mini stroke then show stepped progression, can be slowed by improving cardio as function but after 5 years, 40% die. Have patchy deficits, some areas more affected as receive blood from one artery (frontal lobes as fed by cerebral artery). Means probs conc, confusion, thoughts and behaviour, apathy, restlessness (early than ad), physical weakness

Question 28

Vascular dementia case study: Maggie thatcher

Answer 28

Had series of small strokes, daughter first noticed as was asking same qs often and had to be reminded that husband died

Question 29

Frontotemporal dementia

Answer 29

Rare but common 45-65: no amyloid plaques but have pick bodies inside cells (clumps of abnormal tau) not always. Causes knife edge atrophy (loss of cortex but not white matter). Diff forms depending on location of atrophy- frontal and anterior. Means probs planning, abstract thought, get more reward from sweet food, eat non food objects, change in personality. Become rude, apathetic, impatient, inhibition, empathy, compulsive behaviour and hoarding

Question 30

Semantic dementia (temporal variant FTD)

Answer 30

Atrophy affects anterior temporal lobes bilaterally. Hippo still there but cortex goes (loss of semantic not episodic). Loss of words and pictures, can’t name objects but good language, episodic and verbal reasoning . Can copy picture immediately but after 10s a big diff after 60s so diff (general info but not spec details)

Question 31

Posterior cortical atrophy:focal

Answer 31

Posterior parietal cortex, poor facial recognition, reading and special awareness. Blurred vision, light sensitivity, can’t recognise faces and objects (agnostic), dressing, driving, reading and writing. Memory, lang and thinking fine until later. Breakdown of continuous space, see aspects but not whole picture . Terry pratchett had or- had good spoken language and memory so hid illness

Question 32

Subcortical dementias

Answer 32

Basal ganglia: subcortical structures used in stopping and starting movements and thoughts. Types are Huntington’s (excessive movement) and Parkinson’s (problems initiating)

Question 33

Huntington’s

Answer 33

Genetic disorder dominant mutation of chromie 4, loss of neurones. Early onset 30-45. Restlessness of face, fingers, feet, involuntary movement, poor conc, memory, aggression, depression, lack of eating swallowing and speaking. Basal ganglia inhibits thalamus to cortex connections, HD breakdown pathway affects motor, cog and emotional control. Woody guthrie folk singer, first diagnoses W alcoholism and schizo, correct in 52. Any young 2001: carriers of the gene can’t recognise expression of disgust

Question 34

Parkinson’s

Answer 34

Correlation W age, more common and less heritable than other dementias. Degeneration in substantia nigra in basal ganglia causes deficits in dopamine. Dop suppresses inhibitory loop so releases movement and deficit makes it. Hard to initiate. Develops slowly, no symptoms until dop dropped by 80%(compensation). Treatment is levodopa to boost dopamine.

Question 35

Parkinson’s symptoms

Answer 35

• symptoms: loss of movement (akinesia), can’t generate voluntary movement, including facial expressions (mask face), can’t respond to external stim. Slowness of movement (bradykinesia) slowing of repeated movement like clapping. Disturbed speech. +: tremor at rest, muscular rigidity (agonising pairs tense at same time), involuntary movement. Poor conc, memory, planning, episodic memory example is Micheal j fox: ice hockey stops symptoms

Question 36

Impact of repetitive head injuries

Answer 36

Boxing has repetitive blows to head:chronic traumatic encephalopathy, accumulation of abnormal tau can lead to memory loss, confusion and mood changes but many don’t develop. Amateur boxing wear protection and short fights but not in professional. Boxers are dehydrated if lost weight which reduces cushioning of brain, sparring damages too. Carriers of apeo 4 allele more vulnerable. 5 of World Cup 1996 football team have dementia , neurodegerative risk higher in players but not goalkeepers. But keeping fit reduces risk so less in amateurs and risk lower as not leather balls

Question 37

Malignant social interactions

Answer 37

Make symptoms worse-e.g. deception to get them to engage and treating patients like objects