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Neuroscience Y2S2 > Environment and the Brain 1 > Flashcards

Environment and the Brain 1 Flashcards

1
Q

How are flame retardants suspected to affect IQ? (1)

A

Lower IQ

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2
Q

What event prompted the legislation surrounding flame retardants to be introduced in 1988? (1)

A

Woolworths blaze (1977)

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3
Q

True or false? (1)

By law, all soft furnishings around the world must be treated with flame retardants.

A

False - the legislation has not been implemented in all countries, especially not in Europe

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4
Q

Name the main chemical found in flame retardants which is thought to affect the brain. (1)

A

Bromodiphenyl ether (BDE)

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5
Q

BDE is a ‘forever chemical’.
Give two features of BDE which make it a ‘forever chemical’. (2)

A
  • Little biodegradability
  • Long half-life (>100 days)
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6
Q

Is BDE lipophilic or hydrophilic. (1)

What are the consequences of this? (2)

A

Lipophilic

  • Readily crosses BBB
  • Accumulates in white fat in the body
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7
Q

Describe two specific changes in brain functioning which are thought to be associated with BDE? (2)

A
  • Average decrease in IQ of 3.7
  • Moderate increase in ADHD
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8
Q

Complete the passage relating to BDE exposure and brain development. (3)

BDE exposure begins in utero and has been associated with decrements in ……………………….., …………………….., and …………………………

A

Motor development

Cognitive development

Attention

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9
Q

What two outcomes can be measured to help determine the effects of BDE on brain development? (2)

A
  • BDE-47
  • Neurological outcomes
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10
Q

Give five changes caused by BDE seen during in vitro studies on cultures of cerebellar granule neurones. (5)

A
  • Alterations in signal transduction
  • Oxidative stress
  • Apoptotic cell death
  • Increased ROS
  • Increased reactive carbonyls
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11
Q

Describe a disadvantage of using mice to investigate the effects of BDE on brains rather than humans. (1)

A

Concentrations in man are 10x lower than in mice so results may not be applicable to humans.

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12
Q

Complete the passage relating to white fat in the body. (3)

White fat predominantly acts as an …………………………… in the body, but can also …………….. and ……………….. compounds.

A

Energy store

Absorb

Store

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13
Q

Give seven compounds or groups of compounds which may be absorbed and stored by white fat in the body. (7)

A
  • Vitamins D & A
  • BDE
  • Pesticides
  • Herbicides
  • Organic pollutants
  • Anaesthetics
  • Clinical/recreational drugs
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14
Q

Give three normal/daily activities which may lead to the release of lipophilic compounds in the body. (3)

Why does this happen? (1)

A
  • Exercise
  • Starvation / weight loss
  • Breast feeding

Lipophilic compounds are stored in white fat, and these processes lead to white fat loss and mobilisation of stored compounds.

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15
Q

Complete the passage relating to LogP. (4)

LogP, also called …………….., describes how ………………. a substance is.

It is known as the ……………….. coefficient, and is described by ………………. law.

A

LogKp

lipophilic

partition

Henry’s

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16
Q

Give an equation for Kp and describe this equation in words. (2)

A

Kp = Coil / Cwater

Kp is the solubility of a substance in oil over its solubility in water.

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17
Q

Give an equation for LogP at a given pH. (1)

A

LogP = log10 [octanol]/[water]

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18
Q

Name the substance which makes animal fat appear yellow. (1)

A

beta-carotene

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19
Q

beta-carotene has a LogP of about 11.

Describe what this means in words. (1)

A

The ratio of beta-carotene in fat:plasma is 100,000,000,000:1.

There is 10^11 more beta-carotene in fat than in plasma.

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20
Q

What does it mean if a substance has:

a) a positive LogP
b) a negative LogP

(2)

A

a) substance is lipophilic

b) substance is hydrophilic

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20
Q

Describe the relationship between a substance’s LogP, and how much of that substance will accumulate in white fat. (1)

A

Higher LogP means more of the substance will accumulate in white fat.

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21
Q

What is the approximate LogP value of BDE? (1)

A

6

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22
Q

What value of LogP results in maximum penetration of the blood brain barrier? (1)

A

2-3

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23
Q

Why do molecules with a LogP of <1 not readily cross the BBB? (1)

A

Not sufficiently lipophilic

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24
Q

Why do molecules with a LogP of >4 not readily cross the BBB? (1)

A

They will likely be bound by plasma proteins

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25
Q

Name the simplest route for lipophilic substances to cross the BBB. (1)

A

Transmembrane diffusion

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26
Q

Name four possible routes that lipophobic substances may be able to take in order to cross the BBB. (4)

A
  • Saturable transport (transport proteins)
  • Transcytosis
  • Extracellular pathways
  • Damage
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27
Q

Describe the role of aldehyde dehydrogenase in metabolising dopamine. (1)

A

Metabolises dopamine after MAO (whether MAO or COMT metabolises dopamine first)

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28
Q

Describe the intermediates produced in dopamine metabolism by MAO and aldehyde dehydrogenase. (2)

A

DOPAL produced by MAO metabolism

DOPAL metabolised by aldehyde dehydrogenase to form DOPAC

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29
Q

Give two herbicides/pesticides which have been shown to cause Parkinson’s disease. (2)

A

Rotenone

Paraquat

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30
Q

Where is rotenone naturally found in the environment? (2)

A

Is it a natural product in several tropical and subtropical plants

especially of the Derris genera.

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31
Q

Describe two general uses of rotenone. (2)

A

Pesticide to kill various leaf pests

Piscicide to clear lakes of invasive fish before restocking on fish farms

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32
Q

Rotenone is sold under what brand name? (1)

A

Derris

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33
Q

What is the LogP of rotenone? (1)

What does this mean in terms of its biochemical properties? (1)

A

3.3

It is lipophilic

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34
Q

Does rotenone cross the blood brain barrier? (1)

A

Yes - readily

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35
Q

What is the relative environmental half-life of rotenone? (1)

Give a reason for this half-life. (1)

A

Short (few days)

due to photodegradation

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36
Q

Describe rotenone’s relative potency when acting on neurones in the brain. (1)

A

Very potent (has effects at nanomolar concentrations)

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37
Q

Is the odds ratio of Parkinson’s disease with rotenone use higher or lower than the odds ratio for general pesticide use in farmers? (1)

A

Higher

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38
Q

What is the odds ratio for Parkinson’s disease with rotenone use? (1)

A

OR=2.5

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39
Q

How does rotenone kill cells? (1)

A

Inhibits mitochondrial complex 1

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40
Q

True or false? Explain your answer if appropriate. (1)

Rotenone use has been associated with Parkinson’s disease, but there is little evidence that it is a causal agent.

A

False - it is a known causal agent in PD

Mechanistic causality of neurodegeneration in the SN has been shown.

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41
Q

Rotenone causes neuronal apoptosis.

Give a brain region where rotenone is specifically shown to cause neurodegeneration. (1)

A

Substantia nigra

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42
Q

Rotenone is thought to have a triple effect on substantia nigra neurones to cause cell death.

Briefly give three mechanisms by which rotenone may kill SN neurones. (3)

HINT: It is not inhibiting mitochondrial complex 1 - it is more specific than this

A
  • Reduced ATP production
  • Production of ROS
  • Impaired dopamine metabolism
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43
Q

Describe the chemiosmotic hypothesis of ATP synthesis (the electron transport chain). (5)

A
  • Electrons from NADH and FADH2 passed along proteins of electron transport chain in a series of redox reactions
  • Energy given out by e- movement to gradually lower energy levels
  • This energy is used to pump protons out of the inner mitochondrial matrix to intermembrane space
  • At end of chain, protons travel down concentration gradient through ATP synthase enzyme to produce ATP
  • And oxygen accepts the e- and H+ to form water
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44
Q

Describe the ‘structure’ of the electron transport chain, including where it is found. (2)

A
  • 4 protein complexes and ATP synthase enzyme
  • Which are on the inner mitochondrial membrane
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45
Q

Describe the role of cytochrome C in the electron transport chain. (1)

A

Shuttles electrons between complex III and complex IV

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46
Q

Give two consequences of rotenone blocking mitochondrial complex I of the electron transport chain. (2)

A
  • Inhibition of ATP production
  • Generation of ROS
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47
Q

Describe a potential mechanism by which rotenone-induced block of mitochondrial complex I of the electron transport chain may produce reactive oxygen species. (3)

A

Block of complex I means electrons can’t move down the chain

So they are ‘stuck’ on complex I or in the inner mitochondrial membrane

And may be accepted by O2 to form O2- (superoxide, which is a ROS)

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48
Q

Suggest a mechanism by which ROS produced due to rotenone in cells may be able to induce apoptosis. (1)

A

Via activation of caspase 3

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48
Q

Describe how rotenone is thought to preferentially cause cell death of dopaminergic neurones in the substantia nigra, rather than having equal effects on all neuronal subtypes. (3)

A
  • Rotenone blocks aldehyde dehydrogenase
  • So DOPAL cannot be converted to DOPAC
  • DOPAL builds up in neurones but is highly toxic
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49
Q

Suggest how rotenone causes inhibition of the enzyme aldehyde dehydrogenase. (3)

A
  • Less availability of NAD+
  • Which is a required cofactor for ALDH
  • Due to inhibition of complex 1 by rotenone

(NADH cannot be converted to NAD+ because the electron transport chain is clogged and cannot accept electrons)

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50
Q

Rotenone may kill dopaminergic neurones specifically due to its inhibition of ALDH, which causes a build up of DOPAL in dopaminergic neurones.

Suggest another way in which rotenone may cause DOPAL build up in neurones. (3)

A
  • Rotenone inhibits ATP generation
  • So less ATP available to move dopamine into synaptic vesicles (via VMAT2)
  • So more dopamine in the cytoplasm which is free to be converted to DOPAL
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51
Q

Briefly explain the legislation and control of rotenone use, both as a pesticide and a piscicide. (2)

A

Banned as a pesticide in UK in 2009, and also banned in US, EU, and Switzerland

Still permitted to be used as a piscicide in UK

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52
Q

Rotenone is thought to inhibit aldehyde dehydrogenase by reducing NAD+ availability.

However rotenone also leads to ROS production, which can also inhibit aldehyde dehydrogenase.

Explain how ROS can inhibit aldehyde dehydrogenase. (3)

A
  • ROS cause membrane lipid peroxidation
  • Lipid peroxidation results in aldehyde production
  • So there is competition for the aldehyde dehydrogenase enzyme
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53
Q

State whether rotenone and paraquat are natural or man-made. (2)

A

Rotenone - natural

Paraquat - man-made

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54
Q

Complete the sentence relating to paraquat. (2)

Paraquat is a man-made ………………. which has been used as a ……………………… (brand name Weedol) since the 1950s.

A

oxidant

herbicide

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55
Q

Why is paraquat so useful in industry? (2)

A
  • Cheap way to increase food productivity
  • Cheap method of weed control
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56
Q

Paraquat is a herbicide that can be used on plantation crops globally.

Give six types of plantation crops which paraquat can be used on to increase productivity. (6)

A
  • Maize
  • Oranges
  • Coffee
  • Tea
  • Palm oil
  • Sugar cane
57
Q

How has paraquat use changed in the US since 1992? (1)

A

Increased/tripled

58
Q

Give the logP of paraquat? (1)

What does this mean in terms of its biochemical properties? (1)

A

LogP = -6.7

It is lipophobic

59
Q

How easily does paraquat cross the blood brain barrier. (1)

Suggest a reason why. (1)

A

Cannot readily cross BBB

Because it is lipophobic (LogP=-6.7)

60
Q

Give the relative half-life of paraquat in the environment. (1)

A

Long (>7yrs)

61
Q

Give an effect of paraquat on general health. (1)

How does this tie in with its role in the environment? (1)

A

Systemic poison with no antidote

Which means it is also poisonous to the environment and is able to contaminate soil and water

62
Q

Give a social consequence of paraquat acting as a systemic poison with no known antidote. (1)

A

15-20% of all world suicides are from self-administered pesticide poisoning (such as paraquat)

63
Q

What is the difference between a pesticide and a herbicide? (2)

A

Pesticide is a general term for a substance used to kill animal and plant life

Herbicide is a type of pesticide specific to killing plants/weeds

64
Q

True or false? Explain your answer if appropriate. (1)

Paraquat use has been associated with Parkinson’s disease, but there is little evidence that it is a causal agent.

A

True - a causal mechanism has not been proven

65
Q

What is the odds ratio of Parkinson’s disease with paraquat use? (1)

A

OR=2.5

66
Q

Why do some companies (such as Syngeta, Huddersfield) still use and export Paraquat even though it has been associated with Parkinson’s disease? (2)

A
  • Causality hasn’t been proven (no mechanism has been found)
  • Large commercial interests (cheap way of increasing crop productivity)
67
Q

True or false? Explain your answer if appropriate. (1)

There are multiple civil lawsuits currently in the USA with people claiming that Paraquat has caused their Parkinson’s disease.

A

True

68
Q

Describe why proving mechanistic causality of Paraquat and Parkinson’s disease may be so difficult. (1)

A

Past users of Paraquat (and any other herbicides/pesticides) may be more likely to have other confounding risk factors (perhaps due to occupation), such as being male and smoking.

69
Q

Describe an experimental technique which can show that Paraquat cannot readily cross the BBB. (1)

Describe an issue with this kind of experiment when assessing the effects of Paraquat. (1)

A

PET study using 11C-Paraquat

These are acute studies however paraquat exposure would be long-term, low-dose, chronic exposure

70
Q

It has been shown that an acute dose of Paraquat cannot cross the BBB.

Give two potential mechanisms which may allow long-term, low-dose Paraquat to cross the BBB. (2)

A
  • Paraquat may damage BBB over time to make it leaky
  • A metabolite of paraquat may cross BBB
71
Q

Describe how Paraquat use is controlled over the world. (2)

A

Bans or severe restrictions in 68 countries (not USA)

Banned in UK in 2007

72
Q

Apart from rotenone and paraquat, give another chemical ‘found in your Grandparents’ shed’ which may affect the brain. (1)

A

Trichloroethylene (TCE)

73
Q

Describe the physical appearance of trichloroethylene (TCE). (1)

A

Volatile, colourless liquid

74
Q

Give some current uses of trichloroethylene. (4)

A
  • Degreasers (vapour or cold degreasing)
  • Paint removers
  • Domestic and industrial cleaning agents (such as dry cleaning and carpet cleaning)
  • Textiles (solvent for dyes)
75
Q

Give three things that trichloroethylene (TCE) has been used for in the past. (3)

A
  • Anaesthetic
  • Decaffeination (used as an extraction solvent)
  • Animal feed processing (soybean meal fat extraction)
76
Q

In the past, trichloroethylene (TCE) was used as an anaesthetic.

What was this anaesthetic called? (1)

Why was TCE suitable to be used as an anaesthetic? (1)

A

Trilene

TCE can get into plasma membranes of neurones and impair action potentials

77
Q

Give the LogP of trichloroethylene. (1)

Use the LogP to describe the biochemical properties of TCE. (1)

How does this fit in with its uses in industry? (1)

A

LogP = 2.2

So it is lipophilic

Because of it lipophilicity, it can extract fat from soluble compounds (eg. grease, paint, caffeine)

78
Q

Describe the relative half-life of trichloroethylene (TCE) in the environment. (1)

A

Highly persistent in the environment (so would have a long half-life)

79
Q

Give four ways that organisms can be exposed to trichloroethylene (TCE) in the environment. (4)

A

Water

Food

Breast milk

Air/living space

80
Q

Briefly describe the effects of trichloroethylene (TCE) on the brain. (2)

A
  • Association between TCE and Parkinson’s disease
  • No association with other neurological conditions
81
Q

Briefly describe the mechanism proposed as to how trichloroethylene (TCE) may cause Parkinson’s disease. (5)

A

Similar mechanism to Rotenone

i.e. inhibition of mitochondrial complex 1 in the electron transport chain

Resulting in ROS generation, decreased ATP synthesis, and elevation of toxic DOPAL

and eventually, cell death in the substantia nigra

*TCE-treated brain samples also show a-synuclein inclusions, which are a sign of PD pathology

82
Q

Does trichloroethylene (TCE) act directly on neurones, or does it act indirectly via its metabolites? (1)

A

This is currently unknown

83
Q

Describe an experimental technique which could be used to assess the effect of trichloroethylene (TCE) on neuronal loss in the substantia nigra. (3)

A

Treat subjects or brain slices with TCE or control (if subjects, would have to euthanise and collect brain slices)

Stain brain slices for tyrosine hydroxylase or use fluorogold for retrograde labelling

Assess numbers of cells in substantia nigra pars compacta in TCE-treated vs control brain slices

84
Q

An experiment used tyrosine hydroxylase immunohistochemistry in the substantia nigra pars compacta to assess the effects of trichloroethylene (TCE) on the brain.

What would you expect to see in this experiment? (1)

A

Loss of tyrosine hydroxylase positive dopaminergic neurones in SNc in TCE treated brain, compared to control

85
Q

An experiment used fluorogold retrograde labelling in the substantia nigra pars compacta to assess the effects of trichloroethylene (TCE) on the brain.

What would you expect to see in this experiment? (1)

A

Loss of retrograde-labelled fluorogold dopaminergic neurones in SNc in TCE treated brain, compared to control

86
Q

The effects of trichloroethylene (TCE) on the brain were investigated using male, 5 month old rats, who had received high oral doses of TCE for 6 weeks.

Mitochondrial bioenergetics were measured.

Suggest two ways that mitochondrial bioenergetics can be measured and state exactly what they are measuring. (2)

A

Oxygen consumption (measures oxidative respiration)

Ability to oxidise NADH (measures complex I activity)

87
Q

The effects of trichloroethylene (TCE) on the brain were investigated using male, 5 month old rats, who had received high oral doses of TCE for 6 weeks.

Mitochondrial bioenergetics (oxygen consumption and ability to oxidise NADH) were measured in substantia nigra, striatum, and liver.

Describe and explain the results. (3)

A
  • SN mitochondria show reduced oxygen consumption and reduced ability to oxidise NADH
  • These changes were only seen in SN mitochondria (not striatum or liver mitochondria)
  • Which suggests that TCE selectively inhibits complex 1 of SN mitochondria
88
Q

A 40 year retrospective cohort study was carried out looking at US army veterans with Parkinson’s disease.

Veterans who trained at Camp Lejune had a 70% increased risk of PD compared to those who trained at Camp Pendleton (OR=1.70).

Describe what was found in the study regarding the reasons for higher PD in Camp Lejune veterans. (2)

A
  • Camp Lejune used TCE-contaminated water supply tanks (which contained 70x permitted levels of TCE)
  • TCE runoff from degreasing and machinery cleaning contaminated food, drinking, and bathing water
89
Q

In a study investigating environmental causes of Parkinson’s disease, twin veterans who were discordant for PD were interviewed regarding their previous professions.

What was the outcome/findings of this study? (2)

A

Twins who worked with TCE as a heavy machinery degreaser were at increased risk of PD development

OR=6.1

90
Q

Retrospective studies (ie. looking at people with Parkinson’s disease and then assessing previous environmental exposures or risk factors), provide strong evidence linking trichloroethylene (TCE) use and Parkinson’s disease.

Give a disadvantage of these types of study when investigating causes of Parkinson’s disease. (1)

A

They are able to show association but not causation

91
Q

Describe how organisms can be exposed to trichloroethylene (TCE) in water. (2)

A

TCE is lipophilic so does not dissolve in water

however can attach to organic matter and contaminate water sources

92
Q

Describe the main source of trichloroethylene (TCE) in the air and in living spaces. (1)

A

Fumes from industrial sites

93
Q

Describe the main way by which trichloroethylene (TCE) may get into breastmilk. (1)

Give a further two ways which may contribute. (2)

A

Mothers bathing in contaminated water

Food and drink may also contribute

94
Q

Describe and explain how BMI may affect the concentration of trichloroethylene (TCE) found in breastmilk. (2)

A
  • Women with lower BMIs shown to have higher TCE concentrations in breastmilk
  • Could be due to excess body fat being able to absorb systemic TCE in women with higher BMIs
95
Q

Describe how trichloroethylene (TCE) use is controlled in the US, and EU/UK. (2)

A

CDC in America taking active steps to regulate use of TCE

ECHA (European chemicals agency) reduced and regulated use in EU and UK

96
Q

Describe the general control of trichloroethylene (TCE) use, in terms of:

a) domestic use

b) potential alternatives

c) advertisement

(3)

A

a) domestic use has been regulated

b) other organic alternatives are available and are being used

c) still widely advertised

97
Q

What is a parasite? (1)

A

An organism that lives on or in a host, and survives off or at the expense of its host

98
Q

Are bacteria/viruses classed as parasites? (1)

Explain your answer. (1)

A

No

Because parasites require a living body (host) to survive, and bacteria and viruses can survive outside of the body

99
Q

Name three types of parasite. (3)

A
  • Protozoa
  • Helminths
  • Ectoparasites
100
Q

What is a protozoa, in the context of parasites? (1)

A

One-celled organism such as amoeba or flagellates

101
Q

What is a helminth, in the context of parasites? (1)

A

Multicellular organisms such as parasitic worms

102
Q

What are ectoparasites, in the context of parasites? (1)

A

Parasites which live on the external surface of a host, such as fleas and ticks

103
Q

What is a host, in the context of parasites? (1)

A

The organism on/in which a parasite lives, feeds, and reproduces

104
Q

Give two types of host, in the context of parasites. (2)

Briefly describe these two types of host. (2)

A

DEFINITIVE HOST:

  • host in which the parasite reaches maturity and can reproduce

INTERMEDIATE HOST:

  • host which harbours a sexually immature version of the parasite
105
Q

In the context of parasites, some hosts can also be vectors.

Describe what is meant by a vector. (1)

Give an example of a vector. (1)

A

Can transmit parasites between humans and animals

For example, mosquitoes

106
Q

Name the species of parasite which causes toxoplasmosis. (1)

Describe the species in terms of the following characteristics. (3)

  • Size
  • Single/multicellular
  • Type/category of parasite
A

Toxoplasma gondii

4-8um long by 2-3um wide

Single-celled

Protozoan

107
Q

Describe the relative prevalence of toxoplasmosis infection. (1)

A

Most common human infection worldwide

(1/3 of the world is infected with toxoplasmosis)

108
Q

True or false? Explain your answer if appropriate. (1)

The parasite Toxoplasma bondai, which causes toxoplasmosis, can stay in the body for a lifetime, and people are often infected but do not realise.

A

False - the parasite is called Toxoplasma gondii, however it can stay in the body for a lifetime, and very few people have any symptoms of infection

109
Q

Give two groups of people who may be at higher risk from toxoplasmosis. (2)

A
  • Pregnant women
  • People with a compromised immune system
110
Q

Name the definitive host for toxoplasma. (1)

A

Cats

111
Q

Describe the life cycle of toxoplasma involving cats as the definitive hosts, and intermediate hosts. (5)

A
  • Unsporulated oocysts (which are non-infective) are shed in cat faeces
  • Oocysts sporulate and become infective
  • Infective oocysts taken up by intermediate hosts (eg. birds or mice)
  • Oocysts transform into tachyzoites after ingestion
  • Cats then ingest intermediate hosts as prey and become reinfected
112
Q

When intermediate hosts of toxoplasmosis ingest oocysts from cat faeces, the oocysts transform into tachyzoites.

How to toxoplasma tachyzoites affect the animal which they infect? (2)

A
  • Invade neural tissue and muscle tissue
  • Form cysts of bradyzoites
113
Q

Briefly describe three ways by which humans can be infected with Toxoplasmosis. (2)

A
  • Livestock become infected with sporulated oocysts from cat faeces, and humans then become infected by eating infected, uncooked meat
  • Humans can consume food or water contaminated with cat faeces, or have environmental exposure to cat faeces (such as soil or litterboxes)
  • Blood transfusion or organ transplant contamination is a very rare way for humans to contract toxoplasmosis
114
Q

Briefly explain why pregnant women who have never had toxoplasmosis before have to be very careful not to get it during pregnancy. (1)

A

Pregnant women who contract toxoplasmosis for the first time may pass it onto baby through the placenta

115
Q

What is the most common clinical presentation of Toxoplasmosis infection? (1)

A

Most people have no symptoms of infection

116
Q

Most people with Toxoplasmosis have no symptoms of infection.

However, give three symptoms that may be experienced in a moderate infection. (3)

A
  • Flu-like symptoms
  • Swollen lymph glands
  • Muscle aches/pains
117
Q

Give a group of people who may experience a more severe Toxoplasmosis infection. (1)

A

People with weaker immune systems

118
Q

Fill the gaps relating to Toxoplasmosis. (3)

People with a severe Toxoplasmosis infection may experience damage to ……………….., …………………, as well as other organs, and this happens because ……………………….

A

Brain

Eye

toxoplasma forms tissue cysts

119
Q

Which part of the body is affected by ocular toxoplasmosis? (1)

Give three symptoms that may be experienced with ocular toxoplasmosis. (3)

A

Affects the eyes

SYMPTOMS:

  • reduced/blurred vision
  • Pain (often with bright light)
  • Redness of the eye
120
Q

Describe how toxoplasmosis affects infants who are infected while still in the womb. (2)

A

Most have no symptoms at birth, but may develop symptoms later in life

Small percentage have severe eye or brain damage at birth

121
Q

Describe how the effects of toxoplasmosis on the brain make it more likely that its lifecycle will continue. (3)

A
  • Intermediate animal hosts show reduction in fear and more impulsivity
  • Therefore they are more likely to be preyed on (by cats)
  • Which makes it more likely that cats will become (re)infected and the lifecycle continues
122
Q

Give seven neurological conditions or behavioural changes which have been reported to be associated with toxoplasmosis infection in humans. (7)

A
  • Schizophrenia
  • Bipolar disorder
  • Depression
  • Brain tumours
  • Suicide
  • Road traffic accidents
  • Risk-taking and entrepreneurial activity
123
Q

Very briefly describe the general mechanism by which Toxoplasma infection can cause pathology/changes in the brain. (4)

A

Parasite crosses BBB

in tachyzoite form

and forms cysts in neurones (and muscle cells)

made of bradyzoites

124
Q

Toxoplasma can alter the levels of which specific neurotransmitter in the brain? (1)

Explain 2 ways that this occurs. (2)

A

Dopamine (3x increase)

  • Cysts in neurones express tyrosine hydroxylase
  • Cysts in neurones also express dopamine
125
Q

Toxoplasma may be able to silence neurones in the brain.

Explain how toxoplasma is able to achieve this? (1)

A

Via active manipulation of calcium signalling

126
Q

Give four direct effects/changes seen in brain tissue that has been infected with Toxoplasma. (4)

A
  • Increased dopamine production
  • Functional silencing of neurones
  • Parasites inject parasitic proteins into cells
  • Blocking of apoptosis in neurones where the parasite resides
127
Q

If we disregard the direct alterations that Toxoplasma makes to brain tissue, how else can the Toxoplasma cysts directly affect brain function? (1)

A

Location of the cysts may alter brain function

128
Q

Give four indirect effects of Toxoplasma on brain function. (4)

How do these effects occur, given that they are indirect consequences of Toxoplasma? (1)

A
  • Loss of neurogenesis
  • Increased neurodegeneration
  • Alterations in neurotransmitter balance
  • Loss of synapses and decreased neuroplasticity

These effects occur because Toxoplasma causes low-grade neuroinflammation and activation of microglia and astrocytes

129
Q

Explain how Toxoplasma may be able to cause symptoms in people many years after infection, even if no symptoms were present before. (3)

What symptom/condition does it usually cause? (1)

Who is more susceptible to this process? (1)

A
  • Once the tachyzoite crosses the BBB, it spontaneously differentiates to a bradyzoite form (found in cysts in neurones and muscle cells)
  • Bradyzoites are latent, and persist for a long time, slowly replicating
  • But they can reactivate into virulent tachyzoites

*This would usually cause encephalitis

*Primarily in immunocompromised people

130
Q

Name the organism which is known as the ‘brain-eating amoeba’. (1)

What type of parasite is this? (1)

A

Naegleria fowleri

It is a protozoan parasite

131
Q

Describe the relative prevalence of Naegleria fowleri. (1)

How might this be changing and why? (1)

A

Extremely rare

However may become more common due to climate change

132
Q

Give the three forms that the Naegleria fowleri parasite can be in during its life cycle. (3)

A
  • Cyst
  • Trophozoite
  • Flagellated form
133
Q

Briefly describe the cyst stage of the life cycle of Naegleria fowleri. (1)

A

The parasite forms a cyst to survive in challenging conditions such as low food supply or cold temperatures (below 10oC)

134
Q

Briefly describe the trophozoite stage of the life cycle of Naegleria fowleri. (2)

A

Can actively feed (usually on bacteria)

Can actively replicate

135
Q

Briefly describe the flagellated form of the life cycle of Naegleria fowleri. (2)

A
  • More motile than other forms
  • However when ionic conditions change can convert back into trophozoite
136
Q

Describe the normal ‘habitat’ of Naegleria fowleri. (4)

A

Lives in freshwater such as lakes, rivers, and hot springs.

Grows better in warm conditions up to 46oC.

Also survives in soil.

However cannot survive in salt water so is not found in oceans.

137
Q

Describe how Naegleria fowleri can infect the brains of humans. (3)

A
  • People swim or bathe in lakes and other bodies of water infected with Naegleria fowleri
  • Naegleria enters body through nose (in flagellated form)
  • Attaches to nasal mucosa, passes immune defences, and moves along olfactory nerve (and through cribriform plate and olfactory bulbs) into the brain
138
Q

Describe a feature of Naegleria fowleri parasites which may aid them in getting into the brains of humans. (3)

A
  • Have analogues of ACh receptors
  • So they may react to ACh as a stimulus
  • And follow its release to guide itself into the brain

(Naegleria fowleri follows olfactory nerve, and olfactory bulb receives large ACh input)

139
Q

Name the infection caused by Naegleria fowleri in the brain. (1)

What is the prognosis of this infection? (1)

A

Primary amoebic meningoencephalitis (PAM)

Almost always fatal

140
Q

Give a place in the UK where Naegleria fowleri has been known to inhabit. (1)

A

Roman baths in Bath, England

141
Q

Describe how the Naegleria fowleri parasite causes primary amoebic meningoencephalitis (PAM), and how PAM affects the brain. (6)

A
  • Naegleria fowleri enters brain in trophozoite form
  • Develops 1-12 food cups and eats neurones and astrocytes
  • Also releases cytolytic molecules (acid hydrolases and phospholipases)
  • Tissue destruction causes huge immune response
  • Macrophages and neutrophils infiltrate brain
  • Immune response causes swelling, increased intracranial pressure, and death
142
Q

Naegleria fowleri is also known as the ‘brain-eating amoeba’.

Give two mechanisms that it uses to ‘eat’ brain tissue. (2)

A
  • Develops food cups to ingest neurones and astrocytes
  • Releases cytolytic molecules such as acid hydrolases and phospholipases to destroy tissue

Neuroscience Y2S2 (15 decks)

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