TedTest

From the Ted Talk by Ivan Seah Yu Jun: What is Alzheimer's disease?

Unscramble the Blue Letters

Every four scednos, someone is doaesngid with Alzheimer's dasseie. It's the most coommn cause of dementia, affecting over 40 molilin ppeole worldwide, and yet fiidnng a cure is something that still eludes researchers tadoy. Dr. Alois alhmeiezr, a German pasytshiirct, first described the symptoms in 1901 when he noticed that a particular hospital patient had some peculiar problems, including difficulty sleeping, dtsbeirud memory, drastic mood changes, and increasing confusion. When the patient passed away, Alzheimer was able to do an autopsy and test his idea that perhaps her sotmmyps were caused by irregularities in the brain's structure. What he found beneath the microscope were visible differences in brain tissue in the form of msefdloid proteins called plaques, and neurofibrillary tangles. Those plaques and tangles work together to break down the brain's structure. Plaques arise when another protein in the fttay membrane surrounding nerve cells gets sliced up by a particular enzyme, resulting in beta-amyloid proteins, which are sticky and have a tendency to clump together. That clumping is what forms the things we know as plaques. These clumps block signaling and, therefore, communication between cells, and also seem to trigger immnue reactions that cause the destruction of disabled nerve cells. In Alzheimer's disease, neurofibrillary tangles are built from a protein known as tau. The brain's nerve cells contain a network of tbues that act like a highway for food mleucleos among other things. Usually, the tau protein ensures that these tubes are straight, allowing molecules to pass through freely. But in Alzheimer's disease, the protein collapses into twisted strands or tangles, minkag the tubes disintegrate, obstructing nutrients from reaching the nerve cell and leading to cell death. The destructive piraing of plaques and tangles starts in a riegon cllaed the hippocampus, which is responsible for forming memories. That's why short-term mmeroy loss is usually the first symptom of Alzheimer's. The proteins then progressively iavnde other parts of the brain, creating unique changes that signal various stages of the disease. At the front of the brain, the proteins destroy the atibily to process logical thoughts. Next, they shfit to the region that controls emotions, rilunestg in erratic mood changes. At the top of the brain, they cause paranoia and hallucinations, and once they reach the brain's rear, the pluqeas and tnegals work together to erase the mind's dseepet memories. eutellvany the control centers governing heart rate and breathing are overpowered as well resulting in death. The inlmseemy destructive nature of this disease has inspired many rheecarsres to look for a cure but currently they're focused on slowing its progression. One temporary treatment helps reduce the break down of acetylcholine, an important chemical messenger in the brain which is decreased in Alzheimer's patients due to the death of the nerve cells that make it. Another possible solution is a vaccine that trains the body's immune system to attack beta-amyloid plaques before they can form clumps. But we still need to find an actual cure. Alzheimer's disease was discovered more than a century ago, and yet still it is not well understood. Perhaps one day we'll grasp the exact mechanisms at work behind this threat and a solution will be unearthed.

Open Cloze

Every four _______, someone is _________ with Alzheimer's _______. It's the most ______ cause of dementia, affecting over 40 _______ ______ worldwide, and yet _______ a cure is something that still eludes researchers _____. Dr. Alois _________, a German ____________, first described the symptoms in 1901 when he noticed that a particular hospital patient had some peculiar problems, including difficulty sleeping, _________ memory, drastic mood changes, and increasing confusion. When the patient passed away, Alzheimer was able to do an autopsy and test his idea that perhaps her ________ were caused by irregularities in the brain's structure. What he found beneath the microscope were visible differences in brain tissue in the form of _________ proteins called plaques, and neurofibrillary tangles. Those plaques and tangles work together to break down the brain's structure. Plaques arise when another protein in the _____ membrane surrounding nerve cells gets sliced up by a particular enzyme, resulting in beta-amyloid proteins, which are sticky and have a tendency to clump together. That clumping is what forms the things we know as plaques. These clumps block signaling and, therefore, communication between cells, and also seem to trigger ______ reactions that cause the destruction of disabled nerve cells. In Alzheimer's disease, neurofibrillary tangles are built from a protein known as tau. The brain's nerve cells contain a network of _____ that act like a highway for food _________ among other things. Usually, the tau protein ensures that these tubes are straight, allowing molecules to pass through freely. But in Alzheimer's disease, the protein collapses into twisted strands or tangles, ______ the tubes disintegrate, obstructing nutrients from reaching the nerve cell and leading to cell death. The destructive _______ of plaques and tangles starts in a ______ ______ the hippocampus, which is responsible for forming memories. That's why short-term ______ loss is usually the first symptom of Alzheimer's. The proteins then progressively ______ other parts of the brain, creating unique changes that signal various stages of the disease. At the front of the brain, the proteins destroy the _______ to process logical thoughts. Next, they _____ to the region that controls emotions, _________ in erratic mood changes. At the top of the brain, they cause paranoia and hallucinations, and once they reach the brain's rear, the _______ and _______ work together to erase the mind's _______ memories. __________ the control centers governing heart rate and breathing are overpowered as well resulting in death. The _________ destructive nature of this disease has inspired many ___________ to look for a cure but currently they're focused on slowing its progression. One temporary treatment helps reduce the break down of acetylcholine, an important chemical messenger in the brain which is decreased in Alzheimer's patients due to the death of the nerve cells that make it. Another possible solution is a vaccine that trains the body's immune system to attack beta-amyloid plaques before they can form clumps. But we still need to find an actual cure. Alzheimer's disease was discovered more than a century ago, and yet still it is not well understood. Perhaps one day we'll grasp the exact mechanisms at work behind this threat and a solution will be unearthed.

Solution

people
tangles
fatty
making
ability
deepest
researchers
million
called
region
immensely
pairing
shift
alzheimer
invade
disease
common
memory
tubes
resulting
today
seconds
symptoms
molecules
immune
finding
diagnosed
plaques
psychiatrist
eventually
misfolded
disturbed

Original Text

Every four seconds, someone is diagnosed with Alzheimer's disease. It's the most common cause of dementia, affecting over 40 million people worldwide, and yet finding a cure is something that still eludes researchers today. Dr. Alois Alzheimer, a German psychiatrist, first described the symptoms in 1901 when he noticed that a particular hospital patient had some peculiar problems, including difficulty sleeping, disturbed memory, drastic mood changes, and increasing confusion. When the patient passed away, Alzheimer was able to do an autopsy and test his idea that perhaps her symptoms were caused by irregularities in the brain's structure. What he found beneath the microscope were visible differences in brain tissue in the form of misfolded proteins called plaques, and neurofibrillary tangles. Those plaques and tangles work together to break down the brain's structure. Plaques arise when another protein in the fatty membrane surrounding nerve cells gets sliced up by a particular enzyme, resulting in beta-amyloid proteins, which are sticky and have a tendency to clump together. That clumping is what forms the things we know as plaques. These clumps block signaling and, therefore, communication between cells, and also seem to trigger immune reactions that cause the destruction of disabled nerve cells. In Alzheimer's disease, neurofibrillary tangles are built from a protein known as tau. The brain's nerve cells contain a network of tubes that act like a highway for food molecules among other things. Usually, the tau protein ensures that these tubes are straight, allowing molecules to pass through freely. But in Alzheimer's disease, the protein collapses into twisted strands or tangles, making the tubes disintegrate, obstructing nutrients from reaching the nerve cell and leading to cell death. The destructive pairing of plaques and tangles starts in a region called the hippocampus, which is responsible for forming memories. That's why short-term memory loss is usually the first symptom of Alzheimer's. The proteins then progressively invade other parts of the brain, creating unique changes that signal various stages of the disease. At the front of the brain, the proteins destroy the ability to process logical thoughts. Next, they shift to the region that controls emotions, resulting in erratic mood changes. At the top of the brain, they cause paranoia and hallucinations, and once they reach the brain's rear, the plaques and tangles work together to erase the mind's deepest memories. Eventually the control centers governing heart rate and breathing are overpowered as well resulting in death. The immensely destructive nature of this disease has inspired many researchers to look for a cure but currently they're focused on slowing its progression. One temporary treatment helps reduce the break down of acetylcholine, an important chemical messenger in the brain which is decreased in Alzheimer's patients due to the death of the nerve cells that make it. Another possible solution is a vaccine that trains the body's immune system to attack beta-amyloid plaques before they can form clumps. But we still need to find an actual cure. Alzheimer's disease was discovered more than a century ago, and yet still it is not well understood. Perhaps one day we'll grasp the exact mechanisms at work behind this threat and a solution will be unearthed.

Frequently Occurring Word Combinations

ngrams of length 2

collocation	frequency
nerve cells	4
neurofibrillary tangles	2
tangles work	2

Important Words

ability
acetylcholine
act
actual
affecting
allowing
alois
alzheimer
arise
attack
autopsy
beneath
block
brain
break
breathing
built
called
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cell
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century
chemical
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common
communication
confusion
control
controls
creating
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day
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decreased
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destroy
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destructive
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differences
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disabled
discovered
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disintegrate
disturbed
dr
drastic
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eludes
emotions
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enzyme
erase
erratic
eventually
exact
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find
finding
focused
food
form
forming
forms
freely
front
german
governing
grasp
hallucinations
heart
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highway
hippocampus
hospital
idea
immensely
immune
important
including
increasing
inspired
invade
irregularities
leading
logical
loss
making
mechanisms
membrane
memories
memory
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microscope
million
misfolded
molecules
mood
nature
nerve
network
neurofibrillary
noticed
nutrients
obstructing
overpowered
pairing
paranoia
parts
pass
passed
patient
patients
peculiar
people
plaques
problems
process
progression
progressively
protein
proteins
psychiatrist
rate
reach
reaching
reactions
rear
reduce
region
researchers
responsible
resulting
seconds
shift
signal
signaling
sleeping
sliced
slowing
solution
stages
starts
sticky
straight
strands
structure
surrounding
symptom
symptoms
system
tangles
tau
temporary
tendency
test
thoughts
threat
tissue
today
top
trains
treatment
trigger
tubes
twisted
understood
unearthed
unique
vaccine
visible
work
worldwide