Implications of Tay-Sachs Disease: A Case Study for Public Knowledge

Implications of Tay-Sachs
Disease: A Case Study for
Public Knowledge
By: Adam Green
Wake Forest University
Department of Biology

What am I doing?

 My goals are to explain:
 What is Tay-Sachs Disease?

What am I doing?

 What is Tay-Sachs Disease
 How is it determined?

What I am doing?


 Who can have it and how lethal is it?

What am I doing?

 What are the treatment options?

What am I doing?


 What are the treatment options?
 How can it be prevented?

Patient Case Study and Ethics

 Afterwards, I will present a mock patient case study and
an ethical dilemma.

Interactive Quiz Bowl

 At the end of each section, there will be quiz questions.

Interactive Quiz Bowl

 You will work in teams and you will have two minutes to
answer each question.

Note of Warning

 Before Beginning:
 You should have a competent understanding of DNA,
RNA, and the Central Dogma

Note of Warning

 Genes and the types of mutations

Notes of Warning

 The endomembrane system

Note of warning


 The Plasma Membrane

Notes of Warning
 Plasma Membrane
 Here are some helpful links:
 http://www.ncbi.nlm.nih.gov/Class/MLACourse/Modules/
MolBioReview/slide_list.html
 http://www.youtube.com/watch?v=UAaTEjYmxso
 http://en.wikipedia.org/wiki/Cell_membrane

Let’s Begin!

 Please spilt into teams

What is TaySachs Disease
It is a lysosomal storage
disorder due to genetic
mutations in the HEX A gene.

What is TaySachs Disease?
• One common mutation is a 4
base insertion in the HEX A
gene.

What is TaySachs?
As we know, this could change
how the RNA is transcribed and
the resultant protein.

And in fact, it does change the
protein. The HEX A gene is
responsible for the production
of an enzyme(protein) called βhexsaminidase A that is
responsible for breaking down
fatty substances called GM2
gangliosides that can
accumulate in our brains and
spinal cords.

These enzymes(proteins) are
made on ribosomes attached to
the rough ER and sent to
lysosomes that act as recycling
centers to break down toxic
substances such as fatty
substances called GM2Gangliosidies that accumulate
in our nervous system.
Often lack of function of these
enzymes results in death.

GM2 gangliosides contain a long
hydrophobic tail that inserts
itself into the plasma
membrane of ganglion cells in
neurons surrounding the retina
of our eyes.

Pictures: (top) Hexsaminidase
with both alpha and beta
subunits. Only the alpha
subunit is involved in Tay-Sachs
Disease. (bottom) is a depiction
of a GM2-ganglioside.

They also contain acidic groups
called head groups that stick
above the plasma membrane
and can be involved in cell-cell
recognition as a result.
While the exact function of GM2
Gangliosides is unknown, it has
been suspected that they serve
as an intermediate in the
synthesis of more complex
gangliosides needed for normal
brain development.

This would explain why the
enzyme HEX A cleaves part of
the ganglioside and the
absence of this enzyme results
in improper brain development
often culminating in death.

On another note, this disease is
known as an autosomal
recessive disorder

An autosomal recessive
disorder means that the
mutation in the HEXA gene
exists in two alleles. Alleles are
alternative form of a gene.
Humans contain two sets of
genes, one from their
mother, and one from their
father. The offspring must have
two alleles, one from the
mother and the father, in order
for the disease to be expressed.

The actual enzyme activity
required by β-hexosaminidase
is very small in order to
sufficiently break down GM2gangliosides. Thus, some
individuals may only have one
mutant copy of the HEXA gene.
These individuals will have
abnormally low enzyme activity
levels, but still enough to break
down fatty substances in your
nervous system.
They are called heterozygous
carriers.

If two of these heterozygous
carriers with abnormal enzyme
levels mate, they have a 25%
chance of having a child
affected with Tay-Sachs
Disease. This would mean that
each parent has 1 mutant copy
out of two (1/2) and the child
has both copies; thus the
probability is ½ x ½ = ¼ or
25% that the child will be
affected.
This is the basis for a recessive
disorder.
We see in this family tree, the
offspring ratio is 3:1 and 25%
chance of being affected.

We can also illustrate this
concept through a punnett
square. Lets represent A as the
normal HEX A allele(alternative
form of gene) and a as the
mutant allele that produces
abnormal HEX A enzyme levels.

As you can see, when you cross
two heterozygotes, you get a
25% chance of being affected.

Now, to further complicate
matters, it is important to
realize that more than 120
mutations have been found in
the HEX A gene.
These mutations vary in the
amount of β-hexosaminidase
they produce and thus lead to
less severe forms of the
disease.

This leads to two subtypes of
Tay- Sachs Disease:
1) Early-onset Infantile: the
child possesses two mutant
copies of the HEX A and
produces no functional
enzyme. This the most
severe.

This leads to two subtypes TaySachs Disease:
1) Early-onset Infantile: the
child possesses two mutant
copies of the HEX A and
produces none of the
functional enzyme. This the
most severe.
2) Late – onset adult: disease
caused at times by
compound heterozygosity
that I will explain later.
Patient has abnormal
enzyme levels resulting in
late-onset disease.

The images present a young
child with Tay-Sachs and an
adult with Tay-Sachs

Time for Quiz Questions!!

 Ready your teams!

Quiz Question 1
 The following Base Sequence is the normal gene
sequence: AGTCGTTAACCAG
 Although the above sequence is not the HEX A gene,
what mutational sequence below could be analogous to
Tay-Sachs?
 A. AGTCGTTCAACCAG

 B. AGTCGTTCCAACCAG
 C. AGTCGTTCCGGAACCAG
 D. : AGTCGTTAACCAG

Quiz Question 1

 Time’s up!
 Report your answers

Quiz Question 1
 The following Base Sequence is the normal gene sequence:
AGTCGTTAACCAG
 Although the above sequence is not the HEX A gene, what
mutational sequence below could be analogous to TaySachs?

 A. AGTCGTTCAACCAG
 B. AGTCGTTCCAACCAG
 C. AGTCGTTCCGGAACCAG
 D. : AGTCGTTAACCAG
THE ANSWER is C. A common mutation found in the HEX A
gene can result from a 4 base pair insertion! Give yourself 2
points if you got it right. But note, that other mutations are
also possible.

Quiz Question 2

 Brace yourselves!

Quiz Question 2
 If a male contains one mutant allele for the HEX A gene
(Aa) and the female contains two normal alleles(AA),
then what is the chance that they will have an offspring
with Tay-Sachs? Hint: Draw a Punnett Square.
 A. 75%
 B. 60%
 C. 25%
 D. None of the above

Quiz Question 2

 Time’s up!
 Report your Answers!

Quiz Question 2
 If a male contains one mutant allele for the HEX A gene
(Aa) and the female contains two normal
alleles(AA), then what is the chance that they will have
an offspring with Tay-Sachs? Hint: Draw a Punnett
Square.
 A. 75%
 B. 60%
 C. 25%
 D. None of the above
THE ANSWER IS D. Tay-Sachs is a recessive disorder
meaning that the offspring has to have two mutant alleles.
Only one mutant allele is available. The answer should be
0%.

Question 2: mathematics
explained
Here is an example of how this problem could be solved.
 1) Make a punnett square.

A
A

AA

AA

a


A

Aa

Aa

2)Perform data analysis. For example, we can say that 2/4 of the
offspring or 50% will be heterozygous carriers. The remaining 50%
will be homozygous dominant; thus, since there are no homozygous
recessive offspring, we can say there is a 0% probability of the
offspring having a recessive disease such as Tay- Sachs.

Quiz Question 3


Question 3

 The following blood test was conducted on a patient. The
lab found his β-hexosaminidase levels to be operating at
15%. This means that 15% of the enzymes were
functioning normally. Can we conclude the patient has
Tay-Sachs?
 A. Yes
 B. No
 C. Not sure yet.

Question 3

 Time is up!

Question 3
 The following blood test was conducted on a patient. The
lab found his β-hexosaminidase levels to be operating at
15%. This means that 15% of the enzymes were
functioning normally. Can we conclude the patient has
Tay-Sachs?
 A. Yes
 B. No
 C. Not sure yet.

 THE ANSWER IS B. Remember that the enzyme only
requires small amounts to function normally. This also
ties in to our discussion about different mutations
producing different activity levels. We will discuss more
about “critical thresholds” in the next section.

Tally your scores

 Tally your points. The maximum score is 6 and the
minimum score is 0.

How is TaySachs Disease
determined?
Now that we know what this
disease is. We need to know
how is it determined in the lab.

How is TaySachs
Determined?
Tay-Sachs is primarily
determined by a blood test. An
individual with a family history
of Tay-Sachs can consult their
physician and receive a simple
blood test that measures βhexosaminidase levels.

Determined?
Remember Quiz Question 3?
Well, it turns out that
individuals affected with TaySachs Disease have between
0% activity to 10% activity.
Infantile Tay-Sachs patients
have 0%. Adult patients have
an activity level between 510% to produce symptoms.
Any amount greater than 10%
will result in no symptoms.

How is TaySachs
Determined?
Individuals with blood levels at
or below this “critical threshold
possess visible symptoms such
as:

Determined?
as:
1) Cherry red- spot: results
from the accumulation of GM2gangliosides that can block
blood supply, disrupt a patient’s
vision, and inhibit normal brain
development. Prime indicator of
Tay-Sachs.

Determined?
as:
from the accumulation of GM2gangliosides that can block
blood supply and disrupt a
patient’s vision. Prime indicator
of Tay-Sachs.
2) In children, symptoms arise
within 3 to 6 months. Children
lose motor skills such as the
ability to crawl.

Determined?
as:
from the accumulation of GM2gangliosides lipids that can
block blood supply and disrupt
a patient’s vision. Prime
indicator of Tay-Sachs.
within 3 to six months.
Children lose motor skills such
as the ability to crawl.
3) Eventually, affected
individuals can experience
seizures, paralysis, and loss of
intellectual abilities due to their
nerve cells dying.

Determined?
Individuals with blood levels at or
below this “critical threshold
possess visible symptoms such as:
1) Cherry red- spot: results from
the accumulation of GM2gangliosides lipids that can block
blood supply and disrupt a
patient’s vision. Prime indicator of
Tay-Sachs.
within 3 to six months. Children
lose motor skills such as the ability
to crawl.
3) Eventually, affected individuals
can experience seizures, paralysis,
and loss of intellectual abilities due
to their nerve cells dying.
4) Microscopic Analysis can also
find the retinal neurons to be
bloated from excess ganglioside
storage.

Pictures: The top image represents bloated
retinal neurons from excess ganglioside storage
due to hexosaminidase deficiency.

How is TaySachs
Determined?
My next concern is how can a
mutation or mutations in the
Hex A gene be determined?

How is TaySachs
Determined?
The answer can be solved
through three related
methodologies:
1) PCR

Determined?
The Answer can be solved
methodologies:
1) PCR
2) Gel Electrophoresis

Determined?
The Answer can be solved
methodologies:
1) PCR
2) Gel Electrophoresis
3) DNA Sequencing

Determined?
PCR stands for polymerase
chain reaction. This is done to
amplify a specific segment of a
chromosome such as the HEX
A gene or even a specific
segment of the Hex A gene.
The process can occur in 4 easy
steps:

Determined?
steps:
1) RNA isolation: You have to
isolate the RNA from your
sample and covert it back to
DNA using enzymes known as
reverse transcriptases. This
allows you to only amplify the
region that is expressed.

How is TaySachs
Determined?
steps:
1) RNA isolation: You have to
isolate the RNA from your
sample and covert it back to
DNA using enzymes known
as reverse transcriptases.
This allows you to only
amplify the region that is
expressed.
2) You then apply heat to your
DNA to pull the strands
apart.

How is TaySachs
Determined?
steps:
3) Anneal primers: attach
thermostable DNA sequences to
your DNA to begin the process
of amplification

How is TaySachs
Determined?
steps:
thermostable base DNA
sequence to your DNA to begin
the process of amplification
4) Add a thermostable
polymerase to attach to your
primers and begin replication.

How is TaySachs
Determined?
steps:
thermostable base DNA
sequence to your DNA to begin
the process of amplification
4) Add a thermostable
polymerase to attach to your
primers and begin replication
5) Repeat to desired
amplification.
Picture: Diagram explaining
PCR.

How is TaySachs
Determined?
Now that you amplified DNA,
you can place it on a gel and
run an electric field through
your DNA segment. The
amplified DNA will show up on
the gel and move along the gel
against the negative electrode
since DNA contains negatively
charged phosphate groups.

How is TaySachs
Determined?
Mutant Hex A can be the result
of a 4 base pair insertion; thus,
it would have more phosphate
groups and move less along the
gel than a normal HEX A DNA
due to larger molecules getting
stuck in the gel. Think of the
gel as a sieve.

The following picture is an
example of data from a gel
electrophoresis experiment.
Smaller DNA fragments move
farther than larger DNA
fragments.

How is TaySachs
Determined?
Since Tay-Sachs is caused by
mutations, you can sequence
the HEX A gene of a normal
individual and an affected
individual and see the DNA
change. This is done in two
ways: Sanger Sequencing and
Cycle Sequencing via primers.
Attached are two videos to
watch that explains it in more
detail:

1) http://www.dnalc.org/resour
ces/animations/sangerseq.ht
ml
2) http://www.dnalc.org/view/1
5923-Cycle-sequencing.html
Picture on right depicts Fred
Sanger who developed Sanger
Sequencing. He recently died at
the age of 95.

QUIZ TIME!!

 Now that you understand how mutations in the HEX A
gene can be determined, you can answer these
questions! Ready your troops!

Quiz Question 4:
 A mother reports to her physician that her 4 month year
old just sits in one place for hours with no movement.
She has to be the one to move him at all times. She
suspects he may be paralyzed. What should the doctor
suggest first in his/her diagnosis?
 A. Look for observational clues such as a cherry red spot
 B. Perform a Microscopy Analysis to search for distended
neurons
 C. Order a blood test to look for decreased βhexosaminidase activity levels.
 D. Nothing. The woman is just a paranoid new mother.

Question 4

 Time’s up!!
 Report your Answers!!

Question 4
 A mother reports to her physician that her 4 month year old just sits
in one place for hours with no movement. She has to be the one to
move him at all times. She suspects he may be paralyzed. What
should the doctor suggest first in his diagnosis?
 A. Look for observational clues such as a cherry red spot
 B. Perform a Microscopy Analysis to search for distended neurons
 C. Order a blood test to look for decreased β-hexosaminidase
activity levels.
 D. Nothing. The woman is just a paranoid new mother.
 THE ANSWER IS A. While B and C are also possible, A is a
prime indicator of Tay-Sachs and is the easiest and probably
most convenient way to confirm Tay-Sachs.

Quiz Question 5

 Brace yourselves!!

Question 5

 What feature of DNA structure dictates our rationale that
HEX A mutants with base pair insertions will result in
shorter distances along a gel?
 A. Phosphate groups.
 B. Sugar groups

 C. Base pairs.
 D. acridine ligands

Question 5

 Time’s up!

Question 5
 What feature of DNA structure dictates our rationale that
HEX A mutants with base pair insertions will have
shorter distances along a gel?

 A. Phosphate groups.
 B. Sugar groups
 C. Base pairs.
 D. acridine ligands

 THE ANSWER IS A. While The phosphates in the
DNA backbone contain a negatively charged
oxygen that cause the DNA to repel against the
negative charged electrode, larger DNA fragments
get stuck in the gel more than smaller fragments
and thus move less.

Tally your scores!

 The most points awarded up to this point are 10 points(2
points per question).
 The least points awarded are 0 points 

How lethal is
this disease?
Now that we understand what
Tay-Sachs disease is and how it
can be determined, we still
need to understand one other
factor before we can do a
patient case study. This last
factor is lethality.

How lethal is
this disease?
The most common form of TaySachs disease is infantile TaySachs. Symptoms normally
appear around 3 to 6 months.
The maximum longevity is
sadly only about 4 years or
simply a brief extent into early
childhood.

How lethal is
this disease?
Adult onset disease is more
variable depending on the
mutation and actual amount of
β-hexosaminidase activity
present in the cell.

How lethal is
this disease?
Another factor for adult onset
Tay-Sachs disease is the issue
of compound heterozygosity
that I mentioned previously.

How lethal is
this disease?
Compound Heterozygosity is
just weird. It occurs when an
individual has two recessive
allele mutations in the HEX A
gene at different locations in
the genome. This is indicative
of the fact that there are over
120 mutations found in the HEX
A gene. This can contribute to
adult onset Tay-Sachs as a
result.

How lethal is
this disease?
Another aspect of lethality is
the prevalence.
According to recent studies, 1
out of every 300 people in the
population is a heterozygous
carrier for Tay-Sachs disease.
However, for individuals who
belong to a certain ethnic group
known as the Ashkenazi Jews,
the prevalence increases from 1
in 300 people to 1 in 30 people
who will be a heterozygous
carrier.

Picture on the right depicts
women of Ashkenazi Jewish
heritage. They are genetically
European.

How lethal is
this disease?
The reason why the ratio is so
much greater for Ashkenazi
Jews is likely due to geographic
distributions. A paper published
in the American Journal of
Human Genetics found the
frequency of the HEX A
mutation to be greater in
geographically isolated regions
with the highest frequencies in
countries such as Russia,
Lithuania, and other central and
eastern European countries
where the Ashkenazi Jews
originated. As a result, the ratio
is likely just bad luck.

Figure. The geographic
locations of the Ashkenazi Jews
located in western and eastern
Europe including Russia.

Russia

Quiz Time!!

 Brace yourselves!!

Quiz Question 6
 Which of the following pieces of evidence favors random
“bad luck” for the HEX A mutation in the Ashkenazi
Jewish population?
 A. The ratio for a carrier is 1 out of 30 instead of 1 out of
300.
 B. High mutation frequency in one location and no
frequnecy in other locations.

 C. Heterozygous carriers are capable of producing subnormal enzyme activity levels to prevent symptoms from
appearing.
 D. Some mutations in the HEX A are more deadly than
others.

Quiz Question 6

 Time’s up!!!

Quiz Question 6
 Which of the following pieces of evidence favor random
founder effects over heterozygous advantage for the HEX A
mutation in the Ashkenazi Jewish population?

 A. The ratio for a carrier is 1 out of 30 instead of 1 out of
300.
 B. High mutation frequency in one location and no
frequency in other locations.
 C. Heterozygous carriers are capable of producing subnormal enzyme activity levels to prevent symptoms from
appearing.
 D. Some mutations in the HEX A are more deadly than
others.
 THE ANSWER IS B. Random founder effects occur
from genetic breeding/sampling in isolated
populations over long timespans.

Case Study of Alex

 Now that you understand the basis of Tay-Sachs Disease
 We can examine a mock case study.
 Let’s begin

Meet Alex

 Alex, short for Alexander, is from Russia with two
Russian parents. They are part of the Ashkenazi Jewish
heritage.

Meet Alex

heritage.
 He is 3 months old.

Meet Alex

heritage.
 He is 3 months old.
 Alex is the first child of his parents.

Meet Alex

heritage.
 Alex is 3 months old.
 Alex is the first child of his parents
 A physician observed an eye abnormality called a cherry
red spot through a simple eye examination.

Quiz Question 7


Quiz Question 7

 What should the doctor order based on these
evaluations?
 A. blood test to measure α-hexosaminidase levels.
 B. motor skills test.

 C. Microscopy analysis of bloated nerve cells.
 D. blood test to measure β- hexosaminidase levels.

Quiz Question 7

 Time’s up!

Quiz Question 7
 What should the doctor order based on these
evaluations?
 A. blood test to measure α-hexosaminidase levels.
 B. motor skills test.
 C. Microscopy analysis of bloated nerve cells.
 D. blood test to measure β- hexosaminidase levels.
 THE BEST ANSWER IS D. Currently, the evidence is
strong for Tay-Sachs Disease, but we need to see if the
enzyme activity levels are below the “critical threshold”
levels.

Tally your scores!

 The maximum points possible are now 14 points.

Alex

 The Blood test results are in and the enzyme activity
levels are immeasurable which indicates infantile TaySachs Disease.

Quiz Question 8


Quiz Question 8

 What should the doctor’s next recommendation be?
A. Order the lab to characterize the mutation through PCR
and gel electrophoresis
B. Nothing. The blood test is enough evidence.

C. Contact a genetic counselor
D. Re-run the blood test to confirm accuracy.

Quiz Question 8

 Time’s up!

Quiz Question 8
 What should the doctor’s next recommendation be?
A. Order the lab to characterize the mutation through
PCR and gel electrophoresis
B. Nothing. The blood test is enough evidence.
C. Contact a genetic counselor
D. Re-run the blood test to confirm accuracy.
THE ANSWER IS A. While one blood test is good
evidence, it does not tell us anything about the
genetics of the individual. Thus, it does not inform us
if a mutation is actually present.

Quiz Question 9

 The results are in:

Quiz Question 9

 PCR and gel electrophoresis confirm shorter PCR
products indicating a base insertion.

Quiz Question 9

 DNA Sequencing confirms a 4 base addition for the HEX
A gene.

Quiz Question 8

 DNA Sequencing confirms a 4 base addition for the HEX
A gene.

 This agrees with the blood test and observational clues
to confirm Tay-Sachs Disease.

Quiz Question 9

 Now Brace yourselves!

Quiz Question 9
What are the possible treatment options given this new
diagnosis?
A. Gene therapy approaches that engineer viruses which
will turn the nerve cells into “micro factories” that
produce β-hexosaminidase.
B. Developing synthetic chaperones that guide the βhexosaminidase to fold into its native 3D structure.

C. Replace the β-hexsaminidase enzyme just like diabetics
undergo insulin replacement.
D. Use alternative enzymes that catabolize GM2gangliosides

Quiz Question 9

 Time’s up
 Report your answers!

Quiz Question 9
Patient X

=

 The correct answer is none of
the above. All of the answer
choices exhibit examples of
positive research results, but
they are all still a long away
from actual clinical treatment.
So for now, Tay-Sachs
disease, in particular the
more common Infantile TaySachs Disease is a genetic
death sentence that will shut
down a child’s nervous
system before he/she
reaches kindergarden.

Quiz Question 9

 As a result, when it comes to Tay-Sachs Disease,
especially infantile Tay-Sachs, no one is a winner and
that’s why no points are awarded for this question.

Quiz Question 9

 As a result, when it comes to Tay-Sachs
Disease, especially infantile Tay-Sachs, no one is a
winner and that’s why no points are awarded for this
question.

 Since Alex is afflicted with this disease, he will die and
his parents will be left childless.

Can this disease be prevented or
minimized?

 1) Pre-natal genetic diagnosis: The parents can be
tested to see if they are carriers and if their offspring is
carrying both recessive alleles within 10 to 14 weeks.
The parents could then opt for abortion.

minimized?
tested to see if they are carrier and if their offspring is
 2) Pre-implantation diagnosis: during in vitro
fertilization, you simply discard embryos that test
positive for Tay-Sachs disease.

minimized?
tested to see if they are carrier and if their offspring is
 2) Pre-implantation diagnosis: during in vitro
fertilization, you simply discard embryos that test
positive for Tay-Sachs disease.
 3) 3) Mate Selection: Some Orthodox Jewish groups
such as Dor Yeshorim perform a genetic screening
program that allows couple who test positive as carriers
can avoid conception.

minimized?

 These three strategies are pretty drastic and indicate
that we may still be a while away from actual treatment
options for this rare deadly disease. As a result, these
strategies have presented us with two ethical dilemmas.

Ethical Dilemma?

 Does the current situation make an appropriate case for
abortion given that not all Tay-Sachs patients die in
infancy or childhood?
 In this particular case, is knowledge good, bad, or
ambivalent?

Ethical Dilemma?

 These are the important questions that we must address
and I leave them for you to decide the answer.

Assorted Links and Works Cited
 http://www.cdc.gov/mmwr/preview/mmwrhtml/000383
93.htm

 http://omim.org/entry/272800
 http://link.springer.com/article/10.1007%2Fs00439003-1072-8
 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685578/
 http://www.nature.com/mt/journal/v19/n6/full/mt20112
7a.html
 http://informahealthcare.com/doi/abs/10.1517/1354378
4.10.3.455
 http://www.jbc.org/content/279/14/13478.long

Assorted Links and Works Cited
 http://www.ninds.nih.gov/disorders/taysachs/taysachs.h
tm
 http://ghr.nlm.nih.gov/condition/tay-sachs-disease
 http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH000239
0/
 http://www.genome.gov/10001220
 http://commonhealth.wbur.org/2011/11/tay-sachshuman-trial
 http://newhoperesearch.org/GM2_gangliosidosis.html

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