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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
How do you count neurons?
-the old methods were bad -new methods say, old brains have the same number of neurons as in young brains
26
Do you have changes in the number of neurons in some parts of the brain?
-yes, in the hippocampus but it doesn’t account for the decline in some people
27
How do cognitive skills change in rats?
-age individually -some old ones as good as young
28
What are the differences in young versus old rats?
-differences in hippocampal learning young rats vs old rats -like humans individual variability -some old rats as good as the young
29
Do the worst performing rats have the fewest hippocampal neurons?
-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
Do parts of the hippocampus show minor losses of neurons?
-yes
31
Can decline in cortical performance occur without significant neuron loss?
-yes
32
Is aging a loss of neurons?
-no
33
What changes with age in the brain?
-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
What does not change with age in the brain?
-resting membrane potential -input resistance -spike amplitude and duration -peak magnitude of LTP
35
Does aging affect changes at synaptic level?
-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
What is aging really like?
-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
How is aging specific?
-as each brain is impacted differently, different pathways impacted in different people
38
What is aging about?
-synaptic phenomena not neuronal
39
What is the frontal lobe age-related loss? Is frontal lobe often connected to age related loss? How?
-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
How do you test the prefrontal lobe memory loss in monkeys? (age related)
-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
What is the morphology of the brain in the aged monkeys?
-monkeys with frontal cortex damage most similar to aged monkey
42
What are the frontal cortex age-related changes in monkeys that are old?
-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
What is aging?
-not a single phenomena, individual -few effective interventions
44
What is human memory loss?
-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
What are the changes in normal vs abnormal age related brains?
-age-related mental decline can interfere with normal functioning
46
What is senile dementia?
-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
What is the most common pathological form of senile dementia?
-Alzheimer's disease
48
What is the incidence of Alzheimer's like?
-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
What does Alzheimer's affect?
-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
What is the dramatic difference in abnormal pathological aging?
-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
What is the comparison of an Alzheimer’s and normal brain?
-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
What is the microscopic pathology in Alzheimer's brain?
-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
What occurs first plaques or tangles in Alzheimer’s?
- 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
What is Tau pathology?
-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
What is the plaque made of?
-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
How is Abeta amyloid generated?
- 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
What are some genetic risk factors?
-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
What is the role of ApoE?
-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
What about curing alzheimer's?
-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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