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Flashcards in week 4 Deck (63)
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1

Which amino acid does transcription always start with?

methionine

2

Which post translational modification targets protein for destruction?

ubiquitination

3

Describe lysosomal degradation

long half life
membrane proteins
extracellular proteins

4

describe proteosomal degradation

short half life
key metabolic enzymes
defective proteins

5

Describe primary proteins

sequence

6

describe secondary proteins

local folding

7

describe tertiary proteins

long-range folding

8

describe quarternary proteins

multimeric organisation

9

Describe supra molecular proteins

large scale assemblies

10

What is proteostasis?

protein homeostasis

11

What does proteostasis involve?

synthesis
degradation
localisation
trafficking
assembly
processing
folding

12

Describe alpha helix formation

results from h bonds forming between carbonyl oxygen atom of each peptide bond with the amide H atom from an amino acid 4 positions toward the C terminus

13

Describe an alpha helix

periodic spiral
confers directionality
R groups face outwards, covering the helix

14

Describe beta pleated sheet

each strand is 5-8 amino acid residues
H bonding between strands of polypeptide forms the planar sheey
directionally parallel or anti-parallel
R groups project from both faces of the sheet

15

Describe how secondary proteins form

stabilised by interactions between R groupd
hydrophobic interactions between non-polar R groups
hydrogen bonds between polar R groups
disulphide bonds

16

Describe how proteins normally fold

assemble into 3D conformation
determined by its primary structure
hydrophobicity is an important determinant for final conformation

17

What are some of the problems with protein folding?

considerable variation in time taken for a protein to adapt to final conformation
cellular environment is highly crowded
increased tendency for proteins to aggregate

18

What is a molecular chaperone?

any protein that interacts with, stabilises, or helps another protein to acquire its functionally active conformation, without being present in its final structure

19

how do molecular chaperones work?

selectively bind to short stretches of hydrophobic amino acids

20

What are some proteome maintenance functions of molecular chaperones?

de novo folding
oligomeric assembly
protein trafficking
proteolytic degradation

21

What is the enzyme that detects problems with protein folding?

glucosyltransferase

22

What does glucosyltransferase detect?

hydrophobicity

23

What are the stages of the ubiquitin proteasome system?

polyubiquitination
polyUb- protein recognised by CAP
polyUB removed; protein unfolded
protein threaded through proteasome
proteolysis

24

WHat is a proteinopathy?

accumulation of misfiled proteins resulting in aggregates, thereby gaining toxic activity or losing the normal function

25

What are the genes involved in early onset familial AD?

amyloid precursor protein
presenilin 1, 2

26

What is the gene associated with sporadic AD?

apolipoproteinE e4 allele

27

What are the 2 abnormalities in protein in the brain of someone with AD?

amyloid plaques in extracellular space
neurofibrillary tangles in cytoplasm

28

What is the change in amyloid shape associated with AD?

change from alpha helix to beta sheet

29

What are the main components of neurofibrillary tangles?

paired helical filaments - tau

30

What are the physiological actions of Tau?

neurite outgrowth
axonal transport
microtubule dynamics

31

What are the pathological actions of tau?

neuronal fibrillary tangles
microtubule dysfunction
cell death

32

What are involved on the phosphorylation of tau?

cdk5
GSK3beta

33

What is a proposed mechanism for tau aggregation?

detachment from microtubules
misfiled tau
pretangels
b sheeted sheet containing structures
neurofibrillary tangles

34

Describe dementia with lewy bodies

shares symptoms with AD and parkinson's disease
presence of cortical lewy bodies
alpha - synuclein aggregates

35

Describe a-synuclein in DLB

misfiling into beta pleated sheet structure that further aggregates into higher order insoluble structures; fibrils; the building blocks for lewy bodies

36

Describe transmissible spongiform encephalopathies

family of rare, progressive neurodegenerative disorders
loss of motor control and behavioural changes
can be inherited, sporadic or acquired
long incubation periods
characteristic changes associated with neuronal loss and failure to induce inflammatory resposnse

37

What is anterograde memory loss?

memory loss after disease sets in

38

What is retrograde amnesia?

old memories are forgotten

39

What is aphasia?

loss of language function

40

What is dysphagia?

impaired language function

41

What is agraphia?

loss of ability to write

42

What is alexia?

loss of ability to read

43

What is nominal dysphasia?

trouble naming objects

44

describe wernickes aphasia

fluent, fast, phonemic and semantic paraphasia, comprehension impaired, temporal lobe. receptive dysphasia

45

Describe brocas aphasia

non fluent, agramatic, phonemic paraphasias common, can't get words out, interior frontal lobe. comprehension is in tact

46

Where is important for visuospatial function?

right hemisphere

47

What is topographical disorientation?

dont know way around familiar environment

48

what is agnosia?

non recognition

49

what is prosopagnosia?

doesn't recognise face of people
may recognise smell, style of walking etc

50

What is included in cognition?

attention / orientation
memory
executive functioning
language
calculation
praxis
visuospatial ability

51

What are the different ways that attention can be classified?

arousal
sustained attention
divided attention
selective attention

52

What tests can be used to assess attention?

orientation in time and place
digit span
reciting months of the year backwards
serial 7s
spell world backwards
the STROOP test

53

What is the frontal lobe involved in?

goal setting and motivation
judgement control of inhibtion
flexibility and problem solving
planning / sequencing organisation
abstract reasoning
social behaviour
personality

54

Describe Wernicke's aphasia

fluent
phonemic and semantic paraphasia
comprehension impaired
Wernicke's area (temporal lobe)

55

Describe broca's aphasia

non-fluent
agramatic
phonemic paraphasias common
Broca's area (inferior frontal lobe)

56

What area of the brain is involved in calculation?

left hemisphere
angular gyrus in parietal lobe

57

WHat is acalculia?

inability to comprehend or write numbers properly

58

What is anarithmetria

difficulty with arithmetic

59

What types of dyspraxia are there?

errors in conception
errors in production

60

How can you test praxis?

imitation of gestures
orobuccal movements
use of imagined objects
lower limb apraxia

61

What are common problems associated with visuospatial deficits?

topographical disorientation
difficulties with dressing
mis-reaching for objects
visual neglect
visual object agnosia
prosopagnosia

62

WHat are the hallmark features of delirium?

impaired conciousness
hyperactive or hypoactive subtype
acute onset
change in cognition
visual hallucination
sleep-wake cycle
emotional changes
in most cases, evidence of underlying direct cause

63

What are some of the precipitants of delirium?

infection
stroke
drugs
MI
fractures
cancer
electrolyte/fluid balance problems
heart failure
diabetes
PVD
alcohol withdrawal