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ana 410G > exam 1 learning objectvies > Flashcards

exam 1 learning objectvies Flashcards

1
Q

what is the relationship between electron transport, mitochondrial membrane potential, and proton conductance?

A

as membrane potential decreases:
- proton conductance increases
- ETC increases flow into the cell

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2
Q

what is the relationship between membrane potential, ATP production, ROS production, and mitochondrial calcium cycling

A

as membrane potential increases:
- ROS production increases
- ca2+ cycling increases
-O2 consumption decreases

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3
Q

describe mitochondrial electron transport and ATP production

A
  • Mitochondrial ETC uses redox reactions to drive H+ out of the cell to create an electron gradient
  • ATP is produced by reversing the ETC and pulling H+ into the cell to convert ADP into ATP
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4
Q

what is the mitochondrial theory of aging

A

somatic mutations of mtDNA cause a progressive energy decline leading to death - longer they live, more damage they have, causing death

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5
Q

why do most antioxidants to improve longevity in animals fail?

A

they can’t get through the mitochondrial membrane or can’t get to the exact location they need to get to in order to be functional

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6
Q

what are symptoms of PTSD

A

increased NF-L in CSF, emotional numbing, hyper-arousal (irritability), re-experiencing trauma, shrinkage in HPC

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7
Q

what neuronal brain systems are believed to be involved with PTSD

A

-autonomic activations of norepinephrine (locus coeruleus) and epinephrine release (fight or flight)
- amygdala activation ( hippocampus)
- HPA - crf release by hypothalamus, pituitary releases ACTH, increased cortisol

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8
Q

what are some possible links between TBI and PTSD

A

TBI in severe cases can cause PTSD and both impact stress hormones and can cause elevated HR in post-trauma phase - both have very similar symptoms

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9
Q

why is the military and the world worried about PTSD and why it should be treated

A

high percentages of veterans are diagnosed and those in whole who are diagnosed are 15 fold higher rate of suicide

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10
Q

how does PTSD parallel aspects of neurodegenerative disorders

A

shrinkage in HPC

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11
Q

what is the ratio of neuronal:non-neuronal cells in whole brain? cerebral cortex? rest of brain? cerebellum?

A

Non:Neuronal
whole brain - 1:1
cerebral cortex - 4:1
rest of brain - 11:1
cerebellum - 0.23:1

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12
Q

what is the role of CSF and how does it flow through the CNS

A
  • supports, nourishes, structure, protects
  • lateral ventricles to 3rd (intervertebral foramen) to 4th (cerberal aqueduct)
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13
Q

what are the layers of the brain

A

dura mater, arachnoid mater, pia mater

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14
Q

what is the difference between primary and association areas of the cortex

A

primary cortices are specific gyri dedicated to processing of the signal, association cortices are focused on defining the signal and applying it to create an association with what were experiencing.

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15
Q

what is the blood-brain barrier structure and function

A

capillaries in the brain have tight junctions, pump lipid-soluble substances out, and have carrier-mediated transport to hinder any unwanted toxins from getting into the brain

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16
Q

function of spinal cord

A

receives information from body and sends to muscles, mostly white matter, easily damaged

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17
Q

function of basal ganglia

A

facilitates movement and rich in neurotransmitters (reward pathways)

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18
Q

function of cerebellum

A

coordinates motor activity, easily influenced by drugs,

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19
Q

function of brainstem

A

necessity for living, keeps brain awake,

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20
Q

function of thalamus and hypothalamus

A

“relay station” for cortex, process and filter information, controls endocrine system, motor sensory visual and learning processing

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21
Q

how are the cells in the cerebral cortex layered? which cells are in which layers

A

neocortex is divided into 6 layers (1-6)
- pyramidal cells are in layers 3 and 5
- granule cells are in layers 2 and 4

22
Q

what artery supplies the midlevel subcortical areas?

A

deep branches of the MCA

23
Q

what artery supplies the lateral sides of the cerebral cortex

A

MCA

24
Q

what is the circle of willis

A

an example of collateral circulation as a safety mechanisms for blood flow to continue in an alternate route if an artery’s supply is hindered

25
Q

the ACA supplies

A

the medial aspect of cerebral hemispheres

26
Q

microglia function

A

surveillance cells

27
Q

astrocyte function

A

helping cells - surround synapses to take up Ca2+ and take up/metabolize neurotransmitters

28
Q

what are the 4 types of cells in the brain and what do they do?

A

neurons - signaling (motor,sensory, projection, interneurons)
glia- supporting cells (schwann, microglia, astrocytes, oligodendrocytes
ependymal cells- line cavities to secrete CSF
endothelial- walls of blood vessels

29
Q

characteristics of neurons

A
  • have all same organelles as other cells
  • have lipid bilayer membrane
  • have some specializations
30
Q

what two structures in the roof of the 4th ventricle allow CSF to move into subarachnoid space of spinal chord?

A

median and lateral apertures

31
Q

describe aging of biological systems and why aging is not a disease - theories

A

mutation accumulation, antagonistic pleiotrophy (good genes favored), disposable soma (effective repair)

32
Q

describe major risk factors that accelerate agings

A

dna damage, rna damage, protein damage, membrane damage - random molecular damage causes accumulation of cellular defects and metabolic/genetic factors effect the rate in which disability/disease/frailty from those defects develop

33
Q

what are the strengths and weaknesses of animal models for aging

A

strengths - showed signs of improvement in life span with sir2 gene and treatments
weaknesses - didn’t translate same effect on humans

34
Q

genes implicated with aging are

A

Sir2 gene , Resveratrol, rapamycin, p53 depletion

35
Q

how did caloric restriction play a role in aging with monkey study and BLSA

A

BLSA - found men who tended to live longer shared lifestyles with monkeys who were put on calorie restriction dies (low insulin levels, body temps, higher DHEA levels- adrenal glands and hormones)

36
Q

life span vs life expectancy

A

life span is max years an individual can live, life expectancy is average age the population live to be

37
Q

what are the basic pathological hallmarks of AB and how are they similar or different from other disorders

A

they deposit after being fibrillar and therefore, insoluble. Precursor protein can be impacted by genetics, pathological mutations, aging and can create toxic AB which creates tangles, plaques and disease

38
Q

what is the temporal sequences believed that the different AD characteristics develop

A

APP gets mutated and created insoluble toxic AB which creates tangles, plaques and disease

39
Q

what is AB 40 and 42 and how do they get produced

A

AB40 is the soluble form and AB42 is the toxic insoluble form. AB40 is created when alpha secretase cuts APP off top and gamma secretase cuts CTF leaving AB40 to go off into extracellular space. AB42 is created when a-secretase doesn’t cut the APP off and gamma secretase cuts only the CTF off, then beta secretase comes in and cuts the AB region 2 spots too far down causing insoluble toxic AB42

40
Q

what is tau and why is it more or less important to AD than AB

A

tau is the driving force for symptoms- AB can be present but not present symptoms, tau is more toxic when present - AB added to tau mice kills them but tau has no effect on AB mice

41
Q

what is FAD and how does it relate to AD and models of AD

A

FAD is familial AD and is caused by genetic factors such as ApoE4 and other genetic mutations causing early onset disease. Can see earlier pathology in models with FAD

42
Q

what are generally accepted targets for AD therapeautics

A

presenilin 1 or 2, APP, ApoE4

43
Q

what is the major genetic risk factor late onset sporadic AD

A

ApoE4

44
Q

general overview of gantenerumab, aducanumab, donanemab, and lecanemab drug type and which worked/didn’t

A

Ganterumab - monoclonal antibody improved AB and tau but people declines
aducanumab-strongest phase 2 data but failed in clinical setting and was expensive
- lecanemab -slows progression, works better earlier,
- donanemab - works fastest and most efficiently to reduce pathology

45
Q

key clinical symptoms of ALS

A

muscle atrophy, hyperreflexia, spasticity, fasciculations (tongue twitching), weakness in trunk/limbs

46
Q

describe the regional spread of ALS

A

-spinal cord onset starts in limbs and spreads to trunk and heat
- bulbar onset starts in head/neck and spreads down to trunk and limbs

47
Q

whats the difference between sporadic and familial ALS

A

sporadic ALS is not caused by a genetic factor, familial ALS is caused by a specific gene causing degeneration

48
Q

explain the role of biomarkers in ALS clinical research - give examples

A

biomarkers help to find targets for clinical treatments to focus in on
- Riluzole targets glutamate to inhibit release
- Radicava targets oxidative stressors in free radicals to reduce them
- Relyviro targeted AMX0035 in mitochondria

49
Q

what is the therapeutic role of tofersen in treating SOD1 ALS

A

torfusen antisense oligonucleotide (ASO) that degrades SOD1 mRNA to slow disease progression

50
Q

describe the type of cell at each membrane potential:
- >160mV
- 140-160mV
- 100-140mV
- <100mV

A

160 - resting cell
140-160- normal ATP turnover
100-140 - leaky membrane
100- dead

51
Q

which complex is most susceptible to ROS production

A

complex 1

52
Q

what is a main genetic biomarker for ALS

A

SOD1

ana 410G (11 decks)

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