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Neuroscience > L61 Aging and Alzheimer's Disease > Flashcards

L61 Aging and Alzheimer's Disease Flashcards

1
Q

define a homogenous population

A

populations where people are equally susceptible to injuries, diseases and death

*homogenous population LE = 50 yo
turns out, that the real population curve has a LE of about = 70 yo

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2
Q

why is there an increase in LE?

A

due to ↑medical care and public health

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3
Q

define healthy life expectancy

A

age where seriously debilitating disorders develop

usually 10yrs less than expected life expectancy; thus ppl suffer in their last 10 years

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4
Q

where are regions of highest and lowest LE?

A

western world - highest LE

africa - lowest LE

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5
Q

how does SES affect LE?

A 
↑SES = longer lifespan 
↓SES = shorter lifespan
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6
Q

what can we expect with an increase in LE?

A

incidence of dementia

expected to triples in the next 25 years!

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7
Q

what are included in the “list” of age specific impairments that older people are more susceptible to?

A

SENSORY

  • Visual→ acuity, accommodation and macular degeneration
  • Olfactory→ olfactory neuron loss and damage to olfactory epithelium
  • Hearing→ loss of inner and outer hair cells and spiral ganglion cells
  • Vestibular Apparatus→ degenerative changes at several sites
  • Proprioceptors→ impairment seen particularly in lower limbs

MOTOR

  • Muscle→ loss of mass and replacement with fat deposition
  • Gait→ impairment of gait and postural stability
  • Basal Ganglia→ Parkinsons, Huntingtons
  • Cerebellum→ ataxia’s

COGNITIVE

  • Dementias→ Alzheimer’s, Pick’s Disease
  • Personality Disturbances
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8
Q

what does aging of the nervous system cause? What are the symptoms of brain aging?

A

infirmity

  • Brain weight begins to decline past age-30
  • Fall in neuronal size, dendritic arborization and number of synapses
  • Gyri are smaller and sulci are larger and deeper as cells shrink
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9
Q

what does Aging of the nervous system cause?

A

-losses of function, postural control, gait, reflexes, vision, sleep, memory and general intelligence

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10
Q

what are the possible causes of dementia?

A
  • cerebrovascular disease
  • CNS infection
  • Pernicious anemia – B12 deficiency
  • Folic acid deficiency
  • Wernicke-Korsakoff syndrome
  • tumor
  • trauma
  • neurologic diseases like Huntington’s and Parkinson’s as well as MS

*The most common form of Dementia is Alzheimer’s Disease (dx in 1907) whose cause/origin is uncertain - >50% of dementias

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11
Q

what are the 3 cardinal signs of AD?

A
  1. neuritic senile plaques
  2. neurofibrillary tangles
  3. granulovacuolar degeneration
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12
Q

describe neuritic senile plaques

A

Extracellular spherical deposits containing many neuritic and glial processes with AMYLOID protein core

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13
Q

describe neurofibrillary tangles

A

Intracellular paired helical filaments

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14
Q

describe granulovacuolar degeneration

A

Degeneration caused by formation of intracellular circular clear zones of cytoplasm (vacuolation)

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15
Q

what brain structures are sentile neuritic plaques and neurofibrillary tangles often seen

A 
Hippocampus (CA1)
 neocortex
amygdala
basal forebrain
 locus ceruleus
raphe nuceus
 olfactory cortex
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16
Q

what brain structures are neuron loss most notable in?

A

hippocamps
entorhinal cortex
association cortexes
basal nucleus of Meynert

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17
Q

what neurons does the CNS exhibit selective losses in?

A

noradrenergic, dopaminergic and cholinergic

*limbic system also exhibits pathology

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18
Q

The central core of the neuritic plaques is made of ____ with surrounding parts of damaged neurons

A

amyloid β-protein

19
Q

The APP (amyloid precursor protein) is located in the neuronal _____

A

cell membrane

20
Q

what chromosome codes for APP?

A

chromosome 21

21
Q

What happens to APP in Alzheimer’s brain compared to normal brains?

A

The APP should normally be cleaved by an α-secretase but in this case it is the β or γ-secretase (bad!)

22
Q

what happens as a result of abnormal cleavage of APP like those seen in Alzheimer’s brains?

A
  • Abnormal cleavage of APP results in releae of small peptides in to the ECF
  • Cleavage done by β-secretase and γ-secretase causing the release of Aβ1-40
  • These Aβ molecules aggregate to form these plaques containing axon terminals, migroglia and astrocytes
23
Q

what proteins make up the neurofibrillary tangles?

A

Tau proteins

*Hyperphosphorylated tau proteins in degenerating neurons are the major constituent of these tangles

24
Q

what is the normal function of Tau proteins?

A

form the MAP’s that assist in stabilization and axonal transport for microtubules thus found in high concentration in axons

25
Q

Describe Parkinson’s disease

A
  • Loss of neurons in the Substantia Nigra happens in the 6 to 8 decade
  • Characterized by tremors at rest, akinesia, rigidity, emotional changes and lack of facial expression
  • In addition to depigmentation substantia nigra, LEWY BODIES develop in associated areas including the Substantia nigra, pars compacta, locus ceruleus, basal nucleus of Meynert, raphe nuclei and cerebral cortex
26
Q

describe Lewy Bodies - what they are made of, where they are found.

A

granules (10μm) made mostly of α-synuclein found in presynaptic terminals

27
Q

describe Huntington’s disease

A
  • Typically appears in 5th decade with cognitive and emotional disturbances proceeded by chorea
  • Atrophy of frontal cortices, caudate nucleus and putamen and astrogliosis is evident
  • Marked decreases in GABA and glutamic decarboxylase

Intranuclear and cytoplasmic inclusions/HUNTINGTIN; striatum; frontal cerebral cortex)*

28
Q

Describe ALS

A

-Peaks incidence in 5th decade with intellectual capacity is being retained
-loss of anterior horn cells, motor nuclei of brainstem & UMN loss causing initial weakness in
hands/limbs
-Atrophy of motor neurons, gliosis and extensive loss of myelinated fibers in lateral Corticospinal tract

Bunina bodies/SOD1*

29
Q

Describe Friedrich’s ataxia

A
  • First or second decade, progressive limb an gait ataxia with retained intellectual capacity
  • Loss of deep tendon reflexes and sensory axonal neuropathy
  • Atrophy of dorsal column, Corticospinal tracts and spinocerebellar tracts
30
Q

Describe Pick’s disease

A
  • Onset of 4th/5th decade; early on presents like AD and may be clinically difficult to distinguish
  • Fatal course within 10yrs;; ♀>♂ usually with behavioral disturbances and aphasia
  • Cortical atrophy usually frontal/temporal and unilateral with marked astrogliosis
  • Cytoplasmic inclusions known as Pick Bodies→ densly packed neurofilaments;; distinguishable from AD

***Tau + pick bodies

  • Progressive supranuclear palsy: Neurofibrillary tangles / tau
  • Corticobasal degeneration: Neurofibrillary tangles / tau
  • Frontotemporal dementia: Neurofibrillary tangles / tau

*just because a person has neurofibrillary tangles, doesn’t mean that they will have AD

31
Q

Describe Creuzfeld-Jakob Disease – Prion Disease

A

-Onset of 4th/5th decade but incubation of infectious protein (prion, PrP) may be 10-30yrs
-Fatal w/in 2yrs; three origins→ infection, sporadic or familial (mutation of PrP)
-Pts show dementia, motor weakness, ataxia, tremors, rigidity and myoclonus
-Neuronal loss, astrogliosis and cytoplasmic vacuoles in the cortex and basal ganglia (giving a
spongiform appearance)

32
Q

what is clinically significant about chromosome 21?

A
  • Amyloid gene that encodes the Aβ precursor→ Alzheimer’s Disease
  • Trisomy 21 gives rise to Down’s Syndrome→ if they live past 40 will develop Alzheimer’s Disease
  • link between AD and down syndrome!
33
Q

what is the believe cause of new variant of Creutzfeldt-Jakob disease?

A

-Prion diseases caused by an infectious protein known as a Prion
-caused by eating contaminated beef
from a cow infected with a related animal prion disease known as bovine spongiform encephalopathy

34
Q

Describe Progeria

A
  • Rapid aging in children, evident by age 2 and death b/w 8-21 years of age from heart disease
  • Gene mutation causes defective protein that normally holds nucleus and cell together
35
Q

what is age also a risk factor in?

A

CVD and stroke

36
Q

what are changes seen in AD brain structure?

A
  • Early hippocampal atrophy
  • Brain weight declines
  • Somas, dendrites and number of synapses decline
  • Gyri narrow; sulci, fissures, ventricles & cisterns enlarge
37
Q

what chromosome and gene is associated with late onset AD (sporadic)?

A

chromosome 19 (ApoE/ApoE4)

38
Q

what chromosomes and genes are associated with familial AD?

A

chromosome 1 - PSEN 2
chromosome 14 -PSEN 1
chromosome 21 - APP

39
Q

what chromosome and gene is VERY early onset AD associated with?

A

chromosome 14 - PSEN 1

40
Q

ABeta is ____ to cholinergic neurons

A

neurotoxic

41
Q

What occurs with a gradual accumulation of soluble and insoluble Abeta peptides since Aβ is neurotoxic to cholinergic neurons

A

Cholinergic dysfunction
-diminished acetylcholine release
-impaired coupling of the muscarinic
acetylcholine receptors (mAChRs) to heterotrimeric GTP-binding proteins (G proteins).

42
Q

Prions are also known to be involved with what other diseases?

A
  • Kuru
  • Fatal Familial Insomnia
  • Scrapie in sheep
  • BSE in cattle (“Mad cow disease”)
43
Q

what happens with the conformation of the protein with PrPC –> PrPSc?

A

alpha helix to beta sheet!

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