alzheimers

Question 1

main risk factor and genetic component

Answer 1

age, also mutations eg of APP which cause early onsent alzheimers

Question 2

symptoms of alzheimers

Answer 2

memory loss, confusion, language issues ie stopping in during convo, changes in personality

Question 3

normal processing of APP in healthy ppl with enzymes- AMYLOID hypothesis

Answer 3

amyloid precursor protien (APP) broken by alpha secretase, then into gamma secretase, and product removed

Question 4

pathological processing of APP’s with enzymes- AMYLOID hypothesis

Answer 4

APP broken by BETA secretase (NOT alpha)= beta amyloid protein, which froms clumps around neurones

Question 5

TAU hypthoesis

Answer 5

Tau proteins stabilise microtubues- in alzheimers they hyperphosphorylate and become INSOLUBLE, thus leading to unstable microtubules= neurotoxic

Question 6

inflammation hypothesis

Answer 6

microglia (macrophages of CNS) cause increased release of inflammatory cytokines, more phagocytosis, and less NEUROPROTECTIVE proteins

Question 7

treatment of mild alzheimers- anticholinesterases, which has longest half life, commonality, and differences of drugs

Answer 7

don’t reduce amyloid protein or tau: donepezil- inhibits acetylcholinesterase, with long half life: rivastigmine- inhibits both acetyl and butyrylcholinesterase, which is bad, so given as patch so that only acetyl inhibited: galantimine not only inhibit acetyl, but also a nACHR AGONIST: ALL are REVERSIBLE

Question 8

treatment of ONLY severe alzeihmers

Answer 8

in severe cases, NMDA receptor is OVERACTIVE- memantine blocks glutamate from acting on receptor

Question 9

treatment failures withe examples

Answer 9

gamma secretase inhibitors eg semagacestate, beta amyloid antibodies eg solanezumab, and tau inhibitors eg methylene blue