cycle 9 Flashcards

(12 cards)

1
Q

molecular mechanisms underlying Alzheimer’s Disease

A

formation of beta-amyloid plaques, Tau tangles

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1
Q

structure of neurons and how they communicate at the synaptic cleft

A

structure - microtubules, Tau protein
axon terminal meets dendrites of another neuron.

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2
Q

why cholinergic neurons are downregulated in AD

A

little production of acetylcholine in AD, acetylcholinesterase inhibitors inhibit break down of acetylcholine

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3
Q

molecular mechanism of beta-amyloid plaque formation

A

APP (maintains structure and function of neurons) gets cut in a way that can form clumps which can form plaques

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4
Q

know the molecular mechanism of neurofibrillary tangle formation

A

tau protein holds microtubules together
hyperphosphorylation of tau causes structure to dissociate
neuron dies
tangled tau forms tangle

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5
Q

know the genetic risk factors of AD

A

down syndrome (trisomy 21)
mutations in presenilin 1 and 2
inheritance of Apo E4 (variant of Apolipoprotein E) (Apo E4 not effective at removing Aß aggregates)

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6
Q

difference between inter-tumoural heterogeneity and intra-tumoural heterogeneity

A

inter-tumoural - difference between different tumours from same or different patients
intra-tumoural - differences within a single tumour mass

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7
Q

process of clonal evolution of cancer

A

C required A and B to be mutated before mutating. A and B support C

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8
Q

how certain cancer cells become resistant to drug treatment which leads to relapse

A

chemo is general treatment, targets all rapidly proliferating cells, don’t know where mutation is. second time - different array of heterogeneity

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9
Q

driver mutations vs. passenger mutations

A

driver mutation - pushes clonal evolution, cell to proliferate rapidly
passenger mutation - not contributing to cancer phenotype

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10
Q

difference between proto-oncogenes (RTK) and tumour-suppressor genes (p53) leading to cancer progression

A

proto-oncogenes - growth factor receptors (gain of function mutations), normal genes that become oncogenic if mutated
tumour-suppressor gene - cell cycle checkpoint and DNA repair (loss of function mutations)

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11
Q

role of cancer stem cells in cancer progression and therapy

A

cancer stem cells drive oncogenesis

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