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Sensation, Movement and Complex Functions > Lecture 21- Aging brain > Flashcards

Lecture 21- Aging brain Flashcards

1
Q

What is aging?

A

-Changes in brain function in last few decades of life aging: a bad thing

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2
Q

What are the two types of changes during aging?

A

-normal and pathological

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3
Q

When does the brain change?

A

-alway changing, starts early due to development and plasticity -brain changes constantly from before birth to death

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4
Q

What are the three stages of the brain?

A
  1. Development: setting up the structure of the brain 2. Plasticity: fine tuning, laying down procedural and declarative memories 3. Aging: non-adaptive changes that negatively impact function
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5
Q

When does brain development start?

A

-brain development starts around 3-4 weeks post conceptions

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6
Q

How much does the brain increase in size after birth?

A

-brain size doubles in 9 months after birth

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7
Q

When does the brain reach close to adult size?

A

-reaches 90% of adult size at 6 years

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8
Q

What are the two phases of brain development?

A
  1. In utero 2. After birth
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9
Q

What is the first phase of cortical development?

A
  1. In utero -genetically determined with environmental influences (maternal and fetal) -follows a blue print inherent in the DNA
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10
Q

What is the second phase of cortical development?

A

-cortex becomes sensitive to patterns of sensory stimulation -both spontaneous and after birth externally driven -modulates synaptic connectivity -after birth -brain shaped by experience -period of plasticity

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11
Q

Do different regions mature at different rates?

A

-yes

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12
Q

How does visual cortex mature?

A
  • V1 early maturing path in the brain -primary visual cortex reaches adult thickness at 6 months -when go up, V2 V3 etc takes longer -same for cell density and other structure -visual association areas not at adult state until 10 years
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13
Q

What other regions of the brain take long to mature?

A

-frontal and parietal lobes mature at 11-12 years of age -temporal lobe matures at 16 years

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14
Q

Are there differences between hemispheres in the rates of maturation?

A

-inter-hemispheric differences exist -up to 1 year old, right hemisphere frontal and anterior prefrontal cortex layer V dendrites are longer -by 6-8 years old, left side dendrites become longer

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15
Q

What is synaptic maturation like throughout development?

A

-synaptic density increases to 2 years, reaches peak and then declines over time (visual cortex) -frontal cortex peak at 5 years and then decrease, pruning of not useful connections -maturation sees decrease in synapses -visual cortex maximum at 6 months, declines after 1 year -frontal cortex reaches max at 1 year, adult levels at about 16 years

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16
Q

What is the summary of brain development?

A

-brain continues to develop for a decade and a half, late into adolescence -synapse elimination characterises most of this period -sensory input crucial in structuring and guiding late development

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17
Q

What is aging characterised by?

A

-aging is characterised by negative changes in function -this includes: -motor function -sensory function -sleep -memory -problem solving -some changes due to effector receptor changes (like in the visual system= clouding of the lens)

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18
Q

What are some specific brain functions that don’t change?

A

-vocabulary, information, comprehension

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19
Q

What are some specific brain functions that change during aging?

A

-working memory -long term memory -visuospatial abilities -verbal fluency

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20
Q

Is aging individual?

A

-yes, to an extend -when take a cognitive test, some people don’t decline over the years -cognitive decline is the average, it is not inevitable

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21
Q

Is cognitive decline something that happens in everyone?

A

-on average an age related decline -individually shows a wide range -same for humans and animals

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22
Q

Do individuals age at different rates?

A

-individuals tracked over long periods change cognitive abilities at different rates

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23
Q

What is the cognitive decline in individuals?

A

-some people decline a lot -some maintain their level of cognitive ability

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24
Q

What underlies normal versus pathological cognitive decline?

A

-neurons die, and you have fewer neurons -decline in neurons underlies the cognitive decline -there are fewer neurons in old brains -this is not true!!!

25
Q

How do you count neurons?

A

-the old methods were bad -new methods say, old brains have the same number of neurons as in young brains

26
Q

Do you have changes in the number of neurons in some parts of the brain?

A

-yes, in the hippocampus but it doesn’t account for the decline in some people

27
Q

How do cognitive skills change in rats?

A

-age individually -some old ones as good as young

28
Q

What are the differences in young versus old rats?

A

-differences in hippocampal learning young rats vs old rats -like humans individual variability -some old rats as good as the young

29
Q

Do the worst performing rats have the fewest hippocampal neurons?

A

-count neurons in hippocampus and correlate with performance on maze -do the worst performing rats have the fewest hippocampal neurons -there is no difference in the number of neurons in young and old mice

30
Q

Do parts of the hippocampus show minor losses of neurons?

A

-yes

31
Q

Can decline in cortical performance occur without significant neuron loss?

A

-yes

32
Q

Is aging a loss of neurons?

A

-no

33
Q

What changes with age in the brain?

A

-intensity and frequency simulation needed to evoke LTP increases with age -LTP decays quicker -correlates with poorer performance of aged rats in spatial learning tasks -the LTP decline correlates with decline in performance -LTP- synaptic phenomena so the problem in synapses

34
Q

What does not change with age in the brain?

A

-resting membrane potential -input resistance -spike amplitude and duration -peak magnitude of LTP

35
Q

Does aging affect changes at synaptic level?

A

-yes -entorhinal cortex, fewer inputs to hippocampus than in young animals -this is the operational explanation -entorhinal cortex provides important inputs to hippocampus -these inputs selectively lost in aging -extent of loss correlates with memory deficits in rats

36
Q

What is aging really like?

A

-aging not due to wide spread , nonspecific change across the brain -due to quite specific losses in particular pathways -affects multiple parts of the brain, e.g. frontal lobes

37
Q

How is aging specific?

A

-as each brain is impacted differently, different pathways impacted in different people

38
Q

What is aging about?

A

-synaptic phenomena not neuronal

39
Q

What is the frontal lobe age-related loss? Is frontal lobe often connected to age related loss? How?

A

-frontal lobes support executive function -specific deficits seen with aging in how frontal lobe manipulates memory -can lose source of memory (Where did I learn that?) -can lose specific temporal memory capacity (remembering objects objects in order) -can lose specific temporal memory capacity (remembering objects in order)

40
Q

How do you test the prefrontal lobe memory loss in monkeys? (age related)

A

-test where and when memory -show monkey food being hidden in one of number of possible places -after a delay, let monkey get food (if it can remember) -repeat many times: monkey has to keep last location seen in memory -compare young monkeys with hippocampal or frontal lobe damage with aged monkeys -young monkey do better than older monkeys -old monkey behave like a young monkey with hippocampal or frontal lobe damage

41
Q

What is the morphology of the brain in the aged monkeys?

A

-monkeys with frontal cortex damage most similar to aged monkey

42
Q

What are the frontal cortex age-related changes in monkeys that are old?

A

-no neuron loss in regions responsible for deficits -synaptic density, dendritic architecture and myelination all altered -specific deficits in parts of the frontal cortex not generalised changes

43
Q

What is aging?

A

-not a single phenomena, individual -few effective interventions

44
Q

What is human memory loss?

A

-fMRI/PET shows frontal lobe in aged individuals more affected than hippocampus -emerging view: different parts of the brain age independently with only a broad correlation -unlikely to be a single process underlying all changes

45
Q

What are the changes in normal vs abnormal age related brains?

A

-age-related mental decline can interfere with normal functioning

46
Q

What is senile dementia?

A

-memory loss in an otherwise alert person -loss of at least one other area of cognition, language, problem solving, judgment etc. -may be an inevitable outcome of living a long time, may be pathological

47
Q

What is the most common pathological form of senile dementia?

A

-Alzheimer’s disease

48
Q

What is the incidence of Alzheimer’s like?

A

-rare in sixty -1-3% of 60-70 y.o. -3-12% of 70-80 y.o. -25-35% of over 85 y.o. -early onset forms occur (both sporadic and familial)

49
Q

What does Alzheimer’s affect?

A

-abnormalities common in: -memory -language -problem solving -judgment -calculation -visuospatial awareness -some show psychosis, hallucinations and delusions -end up mute, incontinent and bedridden -diagnose definitively by brain biopsy

50
Q

What is the dramatic difference in abnormal pathological aging?

A

-dramatic neuron and synaptic loss: -neocortex -entorhinal cortex -hippocampus -amygdala -nucleus basalis -anterior thalamus -brainstem -loss of neurons, also synaptic changes -it affects almost all parts of the brain

51
Q

What is the comparison of an Alzheimer’s and normal brain?

A

-massive loss of neurons, it is not standardized loss across the whole brain -hotspots= temporal lobe affected a lot -somatosensory not bad -parietal is bad

52
Q

What is the microscopic pathology in Alzheimer’s brain?

A

-can see tangles and plaques -not clear what they do -independent pieces of pathology -intra neuronal neurofibrillary tangles of tau (microtubule-related protein) -plaques (extracellular deposits of Abeta amyloid)

53
Q

What occurs first plaques or tangles in Alzheimer’s?

A
  • plaques, synaptic loss and tangles precede first clinical signs
  • get as many plaques as you will have before starting to show too bad signs
  • plaques, synaptic loss and tangles precede first clinical signs
  • mild cognitive impairment with full load plaques
  • major brain changes also lag behind
54
Q

What is Tau pathology?

A

-something goes wrong with it and forms a tangle -forms tangles -hyperphosphorylated form of tau -intracellular -exact role unknown -may act synergistically with Abeta amyloid

55
Q

What is the plaque made of?

A

-a beta amyloid -comes from APP, it is in every cell in the body, not clear what it does -we do know that it is cleaved by enzymes and there is one way of cleaving that produces the a beta amyloid -Abeta amyloid comes from amyloid precursor protein -APP is present through neuronal cell membrane and is of unknown function (synapse formation?) -it is cleaved by secretases to produce various sized pieces (Abeta 1-40, Abeta 1-42, and Abeta 1-43) -Abeta 1-42 is toxic and leads to amyloid deposition

56
Q

How is Abeta amyloid generated?

A
  • number of secretases that cleave the APP -the key thing is how long the pink bit is
  • neurons are specieal in that they lack the third enzyme (alpha secretase) which cuts it again and makes it harmless (all other cells have it)
  • 42 amino acid length is the bad
  • aggregates, sticks to itself and forms a plaque
  • alpha secretase present in all cells but neurons cleaves Abeta into harmless fragments
57
Q

What are some genetic risk factors?

A

-makes risk high or low -can have a mutation in APP gene (mutations makes Abeta 1-42 more likely) -can have mutation in Presenilin 1 and 2 that cut the APP (mutation makes Abeta 1-42 more likely) -can also have mutation in Alpha 2 that cleans up the a beta (polymorphism affects Abeta scavenging) -ApoE mutation? not clear why it is connected Apolipoprotein E (ApoE- cholesterol transport) -role of these genes in sporadic late onset Alzheimer’s unclear

58
Q

What is the role of ApoE?

A

-ApoE enhances proteolysis of Abeta -ApoE alleles seems to predict late onset Alzheimer’s -Three alleles: 1: E2- frequency in normal population 0.08 2.E3 (0.78) 3. E4 (0.14) -in late onset Alzheimer’s population E4 is 0.54 -Individuals homozygous for E4 8 times more likely to develop Alzheimer’s than those homozygous for E2 -If no copies of E4 only 20% develop AD, two copies of E4 75-90% develop AD

59
Q

What about curing alzheimer’s?

A

-major challenge for future -no cure, some drugs ease transition into disease state by maintaining function (cholinergic drugs) -research centres on modifying handling of Abeta 1-42 or APP processing -maybe modify action of the modifying genes -some drugs prolong normal function

Sensation, Movement and Complex Functions (22 decks)

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