Reading 2026-09 Test 8 — IELTS Academic Reading Practice Test with Answers

About this set: compiled and lightly cleaned up from real test material that test-takers recalled. IELTS draws from a global question pool, so this material circulates worldwide. To give you a complete, sittable test, material reported around the same period is assembled together — so a set may combine content from several exam dates, not one single sitting. Any audio is a recreation for practice. Organized for study convenience. Based on test-taker recalls — not official IELTS material.

Reading Passage 1: Sorry—Who Are You?

Prosopagnosia is a medical condition that stops people from recognizing people's faces, but how common is it and why does it happen?

(A) It was Jacob Hodes's first day at college. He can still recall spending an enjoyable afternoon being shown around campus by a second-year student named Daniel Byrne, who happened to be from his hometown. Jacob then spent the rest of the year ignoring him. 'I never saw him again,' he says. 'Well, I'm sure I walked past him plenty of times, but I just didn't see him.' This behaviour wasn't intentional. Jacob just couldn't recollect what his fellow student looked like. He had had the same trouble all his life. Friends and relatives would greet him and he would have no idea who they were. It wasn't until five years ago that it all made sense. That was when Hodes was diagnosed with prosopagnosia, a condition that means he is unable to recognise faces. According to researchers, he is far from alone. In fact, the condition is not that uncommon, but until a few years ago only a few dozen cases had ever been described, and all of these had been caused by brain injury. Recently, though, researchers identified a second form of face blindness, developmental prosopagnosia, which is either present from birth or develops very early in life.

(B) In May a team from Harvard University in the US and University College London (UCL) announced the results of a web survey of 1,600 people, suggesting that up to 2 percent of people have some degree of face blindness. Then in August, Martina Gruter and colleagues at the Institute for Human Genetics in Munster, Germany, similarly reported that 2.5 percent of 700 secondary-school pupils they had tested had trouble recognising faces. The results of the surveys took everyone by surprise.

(C) It seems that if you have never known what it is to recognise a face, you don't necessarily know that you are supposed to be able to. Prosopagnosics almost always know that they have trouble recognising people, but they often don't realise that other people have better recognition skills than they do, says Brad Duchaine, a researcher at UCL. Despite these issues, the majority of developmental prosopagnosics possess strategies that allow them to get around their difficulty—for instance, by recognising hair, clothing, or a person's way of speaking—so, unless they see a familiar person out of context, with a new hairstyle or in different clothes, they can recognise people just fine. Even so, the discovery of developmental prosopagnosia has attracted attention from neuroscientists keen to discover what is different about the brain of face-blind people. This difference, they believe, could help solve the problem of how the brain deals with information in general, not just visual data. In other words, it may show whether the brain has specialised parts for specific tasks or is more of a general-purpose information processor.

(D) One issue, however, that will present challenges for researchers is that no two prosopagnosics are the same. Some have problems only with faces, while others have trouble with ordinary everyday objects and, so it turns out, animals which would normally be familiar as well. Some prosopagnosics can train themselves to recognise specific faces; others can't even recognise their own in a mirror. When some have been tested they could identify the emotion that was conveyed on another's face, even though the face itself seemed unfamiliar, while for other subjects this was an impossibility. Some cannot recognise the faces of old friends or fellow students but have no trouble telling whether a particular face from such groups would be attractive to most people. Because of this diversity, working out the cause of prosopagnosia will not be easy.

(E) In Martina Gruter's study, the prosopagnosics who agreed to have their parents and relatives tested reported at least one relative with the condition. Having looked at 38 cases in seven families, the German team believe they have good evidence that a single gene could be responsible. Duchaine also has some evidence that face blindness could be inherited but thinks other factors might be more significant. He refers to studies of babies born with a condition which means the eye's lens is not clear, and when it's the left one, being unable to see through this eye during the first two months of life is a major risk factor for prosopagnosia.

(F) Whatever the cause, what most prosopagnosics want to know is whether they can do anything to improve their face-recognition skills. Joseph DeGutis, a graduate student at the University of California, recently reported successfully training a severe developmental prosopagnosic to recognise faces during tests carried out in the laboratory. The subject also reported that recognising faces in everyday life became easier due to the training. Duchaine now plans to attempt to train sufferers to recognise the five people they most need to know—maybe their immediate family, for example, and essential colleagues. Thomas Gruter, Martina Gruter's husband, who also works on her team, however, is not convinced it will work. 'I don't know how you can have more training than you have already had,' he says. 'Humans already spend all day looking at faces.' He also points out that cheating is a possibility during tests and provides an example. One person we studied said that when she was doing the face-recognition test, she memorised the distance between nose and upper lip. She wasn't the only one. So you can perform well in the test and not do so well in real life.

Questions 1–7

Do the following statements agree with the information given in Reading Passage 1?

In boxes 1–7 on your answer sheet, write

TRUE if the statement agrees with the information

FALSE if the statement contradicts the information

NOT GIVEN if there is no information on this

1
Before attending college, Jacob was capable of recognising people he knew well.
- A. TRUE
- B. FALSE
- C. NOT GIVEN
2
Researchers believe that prosopagnosia may be a growing problem.
3
It is harder to identify developmental prosopagnosia in babies than in young children.
4
A German study seems to support the Harvard and UCL research findings.
5
In general, prosopagnosics are aware that other people can recognise faces more easily than they can.
6
In most cases, prosopagnosics have developed ways to deal with their problem.
7
The study of prosopagnosia may help neuroscientists to treat different kinds of brain injury.

Questions 8–13

Complete the notes below.

Choose ONE WORD ONLY from the passage for each answer.

Write your answers in boxes 8–13 on your answer sheet.

The challenges for prosopagnosia researchers

Differences in prosopagnosics

As well as being unable to recognise facial features, prosopagnosics may also have problems recognising

commonly seen (8) ________ and objects

the (9) ________ on someone else's face

Some prosopagnosics can recognise that people are regarded as attractive by others.

Causes of prosopagnosia

Prosopagnosia may be caused by

just one (10) ________, according to Martina Gruter

a defect in the (11) ________ eye, according to Brad Duchaine

Treatment for prosopagnosia

Joseph DeGutis's patient proved he had been successfully trained to recognise faces inside the (12) ________ and in the outside world.

Duchaine's training may allow prosopagnosics to recognise faces belonging to family and workmates.

Thomas Gruter doubts that the training will work and mentions that (13) ________ by some subjects can affect research results.

Reading Passage 2: Muscle Loss

For people confined to bed for long periods of time, or for astronauts in microgravity, muscle wasting is a serious problem. Wasting, or atrophy, is a symptom not only of disuse and injury, but of many diseases, including kidney failure, cancer and AIDS. Once enough muscle has been lost, a vicious cycle sets in as exercise becomes increasingly difficult, which in turn leads to disuse and further atrophy.

Despite more than three decades of research into alternatives, the only way to stop such patients losing muscle is a long course of physiotherapy involving weight-bearing exercise, but this is of little use to the weakest and sickest—and in most cases, starts only after wasting has already set in. The use of anabolic steroids is being explored for some conditions. But these compounds have a huge range of effects on the body besides promoting muscle growth, some of them undesirable, and only appear to work well in conjunction with exercise.

Alfred Goldberg, a cell biologist at Harvard University, began studying muscle atrophy in the late 1960s. What he and others discovered was that, rather than being a passive side effect of disuse or disease, muscle wasting is an active process controlled by a complex genetic pathway. So, if someone found out how it was turned on, it ought to be possible to turn it off. “Back then we didn't know the pathway for muscle breakdown,” says Goldberg, “but about five years ago our work showed that no matter what the trigger—disuse, metabolic disease or fasting—the same biochemical programme is responsible.”

The process involves the ubiquitin-proteasome pathway (UPP), the disposal machinery used to break down unwanted proteins in the cell. Once the system has been activated, ubiquitin “destroy me” labels are added to muscle proteins. This breaks down the muscle filaments within cells, but does not change the number of muscle cells. Instead, they become thinner and weaker. Further studies showed that at least 90 genes are involved in atrophy; Goldberg calls them “atrogenes.” Although it is still unknown which of these genes triggers atrophy, it soon became clear that two of them are essential to the process. Atrogin1 and muRF1 were first described in 2001 and are the only two atrogenes active only during muscle atrophy. They code for ubiquitin ligases, the enzymes that attach the “destroy me” labels to proteins. The genes are barely active in normal muscle, but expression levels shoot up in sick animals. Knock out either, and muscle wasting all but stops.

An experiment was conducted on a “superboy” who was normal at birth, lacking fat; by the age of five, he was excellent at weightlifting, lifting as much as three kilograms. The scientists found that this is closely related to his mother, who is a professional runner, and that his extended family has unusually strong abilities. The boy's condition is caused by a lack of myostatin, a protein that normally limits muscle growth. Without it, muscles grow far larger and stronger than usual. But the drug can have a temporary effect.

There are still many gaps to be filled in, but those in the field agree that the question is no longer if we can develop anti-wasting treatments, but when. As researchers close in on this target, excitement is mounting about exactly what such treatments could achieve. Patients due to be confined to bed for more than a few days could be given the drug as soon as they begin bed rest to prevent muscle loss that would otherwise slow their recovery. Weaning patients off respirators would become easier as doctors could prevent wasting of the diaphragm. Disease need no longer lead to weakness, and broken bones would not mean long and painful physiotherapy sessions to rebuild muscle strength. And since loss of muscle mass is a major reason why we grow frail with age, an anti-wasting drug could keep older people on their feet and living independently for longer.

The prospect of preventing atrophy is also of great interest to NASA, particularly in view of its much talked-about mission to Mars. By the time astronauts reach the Red Planet, they can expect to lose up to 25 per cent of their muscle mass and be too weak to walk, let alone put on a space suit and carry out repairs. That is why Goldberg's work is funded by the National Space Biomedical Research Institute in Houston, Texas, set up by NASA.

While there are valid medical and space applications for anti-wasting drugs, as a safer alternative to steroids they will inevitably be hugely tempting for athletes too, not to mention the lazy as well. Although Goldberg is keen to point out that helping cheats and couch potatoes is not the focus of his work, he admits that it will undoubtedly happen sooner or later.

Questions 14–19

Reading Passage 2 has eight paragraphs, A–H.

Which paragraph contains the following information?

Write the correct letter, A–H, in boxes 14–19 on your answer sheet.

14
A description of a boy with unusual muscle strength
15
A reference to the limitations of current treatments for muscle loss
16
A mention of a space agency's interest in anti-wasting research
17
A reason why space travel could lead to severe muscle loss
18
An explanation of the biological process that causes muscle breakdown
19
A prediction of the wide-ranging benefits of anti-wasting drugs

Questions 20–21

Choose TWO letters, A–E.

Write the correct letters in boxes 20 and 21 on your answer sheet.

20–21
Which TWO statements are true about the genes Atrogin1 and muRF1?
- A. They are active in normal muscle tissue.
- B. They are only active during muscle atrophy.
- C. They prevent the breakdown of muscle proteins.
- D. They are responsible for producing muscle filaments.
- E. They code for enzymes that label proteins for destruction.

Questions 22–26

Complete the summary below.

Choose ONE WORD ONLY from the passage for each answer.

Write your answers in boxes 22–26 on your answer sheet.

The study of the “superboy” revealed he had very little (22) ________ at birth. By the age of five, he could lift up to (23) ________ kilogram(s). His mother works as a (24) ________, and other members of his family have (25) ________ great strength. This condition is linked to a lack of (26) ________.

Reading Passage 3: Synaesthesia

(A) Imagine a page with a square box in the middle. The box is lined with rows of the number 5, repeated over and over. All of the 5s are identical in size, font and colour, and equally distributed across the box. There is, however, a trick: among those 5s, hiding in plain sight is a single, capital letter S. Almost the same in shape, it is impossible to spot without straining your eyes for a good few minutes. Unless that is, you are a grapheme–colour synaesthete – a person who sees each letter and number in different colours. With all the 5s painted in one colour and the rogue S painted in another, a grapheme–colour synaesthete will usually only need a split second to identify the latter.

(B) Synaesthesia, loosely translated as “senses coming together” from the Greek words syn (“with”) and aesthesis (“sensation”), is an interesting neurological phenomenon that causes different senses to be combined. This might mean that words have a particular taste (for example, the word “door” might taste like bacon), or that certain smells produce a particular colour. It might also mean that each letter and number has its own personality—the letter A might be perky, the letter B might be shy and self-conscious, etc. Some synaesthetes might even experience other people’s sensations, for example feeling pain in their chest when they witness a film character gets shot. The possibilities are endless: even though synaesthesia is believed to affect less than 5% of the general population, at least 60 different combinations of senses have been reported so far. What all these sensory associations have in common is that they are all involuntary and impossible to repress and that they usually remain quite stable over time.

(C) Synaesthesia was first documented in the early 19th century by German physician Georg Sachs, who dedicated two pages of his dissertation on his own experience with the condition. It was not, however, until the mid-1990s that empirical research proved its existence when Professor Simon Baron-Cohen and his colleagues used fMRIs on six synaesthetes and discovered that the parts of the brain associated with vision were active during auditory stimulation, even though the subjects were blindfolded.

(D) What makes synaesthesia a particularly interesting condition is that it is not an illness at all. If anything, synaesthetes often report feeling sorry for the rest of the population, as they do not have the opportunity to experience the world in a multisensory fashion like they do. Very few drawbacks have been described, usually minimal: for instance, some words might have an unpleasant taste (imagine the word “hello” tasting like spoilt milk), while some synaesthetes find it distressing when they encounter people with names which do not reflect their personality (imagine meeting a very interesting person named “Lee”, when the letter E has a dull or hideous colour for you—or vice versa). Overall, however, synaesthesia is widely considered more of a blessing than a curse and it is often linked to intelligence and creativity, with celebrities such as Lady Gaga and Pharrell Williams claiming to have it.

(E) Another fascinating side of synaesthesia is the way it could potentially benefit future generations. In a 2013 study, Dr Witthof and Dr Winawer discovered that grapheme-colour synaesthetes who had never met each other before experienced strikingly similar pairings between graphemes and colours—pairings which were later traced back to a popular set of Fischer-Price magnets that ten out of eleven participants distinctly remembered possessing as children. This was particularly peculiar as synaesthesia is predominantly considered to be a hereditary condition, and the findings suggested that a synaesthete’s environment might play a determining role in establishing synaesthetic associations. If that was true, researchers asked, then might it not be possible that synaesthesia can actually be taught?

(F) As it turns out, the benefits of teaching synaesthesia would be tremendous. According to research conducted by Dr Clare Jonas at the University of East London, teaching people to create grapheme-colour associations the same way as a synaesthete may have the possibility to improve cognitive function and memory. As she put it, ‘one possibility is guarding against cognitive decline in older people—using synaesthesia in the creation of mnemonics to remember things such as shopping lists.’ To that end, researchers in the Netherlands have already begun developing a web browser plug-in that will change the colours of certain letters. Rothen and his colleagues corroborate the theory: in a paper published in 2011, they suggest that synaesthesia might be more than a hereditary condition, as the non-synaesthetic subjects of their study were able to mimic synaesthetic associations long after leaving the lab.

(G) There is obviously still a long way to go before we can fully understand synaesthesia and what causes it. Once we do, however, it might not be too long before we find out how to teach non-synaesthetes how to imitate its symptoms in a way that induces the same benefits 4.4% of the world’s population currently enjoy.

Questions 27–33

Reading Passage 3 has seven paragraphs, A–G.

Which paragraph contains the following information?

Write the correct letter, A–G, in boxes 27–33 on your answer sheet.

27
some of the disadvantages related to synaesthesia
28
what scientists think about synaesthesia’s real-life usefulness
29
a prediction for the future of synaesthesia
30
an example of how grapheme-colour synaesthesia works
31
a brief history of synaesthesia
32
some of the various different types of synaesthesia
33
information about a study that suggests synaesthetic symptoms are not arbitrary

Questions 34–37

Do the following statements agree with the information given in Reading Passage 3?

In boxes 34–37 on your answer sheet, write

TRUE if the statement agrees with the information

FALSE if the statement contradicts the information

NOT GIVEN if there is no information on this

34
There are 60 different types of synaesthesia.
- A. TRUE
- B. FALSE
- C. NOT GIVEN
35
Before Professor Simon Baron-Cohen’s research, synaesthesia was thought to be a myth.
36
A lot of celebrities are affected by synaesthesia.
37
Most scientists believe that synaesthesia runs in families.

Questions 38–40

Complete the summary below.

Choose ONE WORD ONLY from the passage for each answer.

Write your answers in boxes 38–40 on your answer sheet.

Synaesthesia is a unique neurological condition that causes different senses to get mixed. Recent research has suggested that teaching synaesthesia to non-synaesthetes can enhance (38) ________ and guard against the deterioration of cognitive (39) ________; unfortunately, it might be a while before we come up with a beneficial way to (40) ________ it to the general population.

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1. B
The passage says Jacob could not recognise people he knew well before college, so the answer is FALSE.
2. C
There is no information about whether researchers think prosopagnosia is becoming more common, so the answer is NOT GIVEN.
3. C
The passage does not compare how hard it is to identify developmental prosopagnosia in babies versus young children, so the answer is NOT GIVEN.
4. A
The passage says a German study supports the findings from Harvard and UCL, so the answer is TRUE.
5. B
The passage says most prosopagnosics are not aware that others can recognise faces more easily, so the answer is FALSE. The tempting wrong answer is TRUE, but the passage clearly says the opposite.
6. A
The passage says most prosopagnosics have developed coping strategies, so the answer is TRUE.
7. C
There is no information about whether studying prosopagnosia will help treat other brain injuries, so the answer is NOT GIVEN.
8. animals
9. emotion
10. gene
11. left
12. laboratory
13. cheating
14. E
Section E describes a boy with unusual muscle strength, so the answer is E.
15. B
Section B talks about the limitations of current treatments for muscle loss, so the answer is B.
16. G
Section G mentions a space agency's interest in anti-wasting research, so the answer is G.
17. A
Section A gives a reason why space travel could lead to severe muscle loss, so the answer is A.
18. D
Section D explains the biological process that causes muscle breakdown, so the answer is D.
19. F
Section F predicts the wide-ranging benefits of anti-wasting drugs, so the answer is F.
20. B / E
The passage says Atrogin1 and muRF1 are only active during muscle atrophy (so B is correct) and they code for enzymes that label proteins for destruction (so E is correct). The tempting wrong answer A is incorrect because they are not active in normal muscle tissue.
21. B / E
22. fat
23. three / 3
24. runner
25. unusually
26. myostatin
27. D
28. F
29. G
30. A
31. C
32. B
33. E
34. B
35. C
36. C
37. A
38. memory
39. function
40. teach

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Reading Passage 1: Sorry—Who Are You?

Reading Passage 2: Muscle Loss

Reading Passage 3: Synaesthesia

Answer sheet

Answer key