IELTS Academic Reading Practice Test 364

On 25 November 1901, a woman of 51 was brought to the municipal asylum for the insane and epileptic in Frankfurt, Germany. Her name was Auguste Deter. She had become impossible to care for at home: she forgot things within minutes, lost her way inside her own flat, and could no longer read or write. Her husband, Karl, could no longer manage, and she was admitted as a patient. The doctor who took charge of her case was a 37-year-old psychiatrist named Alois Alzheimer.

Alzheimer had been born in 1864 in the Bavarian town of Marktbreit, the son of a notary. He studied medicine at Berlin, Tübingen and Würzburg, qualifying at Würzburg in 1887 with a dissertation on the glands of the ear. He then joined the staff of the Frankfurt asylum, where he remained for fourteen years, and became known for his skill in examining brain tissue under the microscope. Colleagues remembered him as a meticulous clinician who recorded every detail of his patients' behaviour, and it was this habit that turned the Deter case into one of the most closely documented in the history of medicine.

Her illness was unlike ordinary forgetfulness. Her memory for recent events had almost gone, yet she could still give her own first name. She was frightened and suspicious: at night she would shout for hours, and she accused her husband of stealing her possessions and of being unfaithful. She had difficulty writing her name. Alzheimer tested her repeatedly, asking her to name objects, to spell words and to say where she was. She could not say how long she had been in the institution, or whether she had been there for weeks or for months, and she was, by the standards of the time, unusually young for such severe symptoms.

According to the notes he kept, when he asked her what she was doing she replied that she had lost herself, and when he asked what she was looking for she said that she did not know. Asked for her surname, she gave her first name instead. Over the following years her condition worsened, and she lost most of her remaining abilities. Alzheimer's file on her contained pages of such exchanges, written in his own hand; when he later became known for his work on the disease, these notes became one of the few sources of information about its earliest stages.

Alzheimer left Frankfurt in 1903 to take up a post in Munich, where Emil Kraepelin had gathered a group of researchers at the university's psychiatric clinic. He did not forget his former patient. When Auguste Deter died on 8 April 1906, at the age of 55, her brain was sent to Munich at his request. There, using a silver staining technique that made individual nerve fibres visible under the microscope, he examined thin sections of her cortex. The tissue showed changes that he had not seen before.

On 3 November 1906, Alzheimer described the case to a meeting of south-western German psychiatrists in Tübingen. He reported that the cortex was thinner than normal and that nerve cells had disappeared from many areas. He also pointed to two kinds of deposit: small structures lying between the cells, which he called miliary foci, and thickened bundles of fibres within the cells themselves. Accounts of the meeting suggest that his talk drew little response, and the minutes record no discussion of the case at all. Most of his audience probably regarded it as a curiosity rather than as a new disease.

The following year he published a fuller account in a German psychiatric journal. He was able to describe the two kinds of change in detail, but he could not explain what caused them or how they were related. The deposits he had seen are now known as plaques, and the fibres as tangles; both remain the defining features of the illness. Because Deter was only 51, her case did not fit the accepted view that dementia belonged to old age, and some of Alzheimer's colleagues doubted that they were looking at a separate disease at all.

It was Kraepelin, by then the most influential psychiatrist in Germany, who settled the matter, giving the condition the name Alzheimer's disease in the eighth edition of his widely used textbook, published in 1910. Alzheimer himself did not live long enough to see the illness become a major field of research: he died in December 1915, aged 51.

The patient was largely forgotten. Then, in the 1990s, Konrad Maurer, a professor of psychiatry at the Frankfurt hospital where Deter had been treated, and his colleagues searched its archive and found her medical file, which had survived the century. Slides of her brain tissue, preserved in Munich, were also traced and re-examined, and modern techniques confirmed that the changes Alzheimer had described were the same plaques and tangles that pathologists now look for. Alzheimer's disease, the commonest cause of dementia, now affects tens of millions of people worldwide, and the question of what produces the plaques, and whether they cause the illness or result from it, is still argued over more than a century later.

It is often said that the brain begins to decline from the moment we reach adulthood. The reality is more complicated. Imaging studies consistently show that the brain loses volume as people grow older, but the loss is uneven, and the age at which it begins varies from one region to another. Some abilities, including vocabulary and general knowledge, often hold up well into the seventies or beyond, while others, such as the speed at which information is processed, begin to slip much earlier. The task facing researchers is to separate the changes that are a normal part of ageing from those that signal disease.

Overall, the brain shrinks by roughly five per cent in volume for every decade after the age of forty, and the loss accelerates in later life. The shrinkage is not simply a matter of cells dying. The ventricles, the fluid-filled spaces at the centre of the brain, widen as the tissue around them contracts. The prefrontal cortex, a region at the front of the brain involved in planning, decision-making and controlling impulses, loses tissue steadily, and the hippocampus, which is essential for forming new memories, also shrinks. The cerebellum, the structure at the back of the brain responsible for balance and coordination, holds up relatively well.

The idea that we lose thousands of neurons every day, once repeated in textbooks, has not survived careful counting. Modern stereological methods, which estimate cell numbers from thin slices of tissue rather than from single microscope fields, suggest that the loss of neurons in the cortex is modest in normal ageing. What appears to decline more sharply is the network of connections between cells: synapses, dendrites and the branches that link one neuron to another. Some studies have reported that surviving neurons can grow new branches, which may offset losses elsewhere. The brain's hardware, in other words, is largely preserved while its wiring becomes less efficient.

One of the most noticeable changes is a general slowing down. Older adults typically take longer to react, to retrieve a name or to switch between two tasks. Timothy Salthouse, a psychologist who has studied cognitive ageing for decades, argues that this slowing is not merely one symptom among many but the root cause of much else. In his view, when mental operations take longer, the products of those operations decay before they can be used, so that memory and reasoning suffer as a consequence. The slowing has been linked to the deterioration of myelin, the fatty sheath that insulates the brain's white matter and allows signals to travel quickly along nerve fibres.

Yet the ageing brain is not simply a younger brain that has worn out. One influential account, the scaffolding theory of ageing and cognition, proposed by Denise Park and Patricia Reuter-Lorenz, holds that the brain responds to decline by recruiting additional regions to help with a task. Brain scans support the idea: whereas young adults typically use one hemisphere for a particular task, older adults frequently activate regions on both sides. This extra activity is not always helpful, since it can reflect confusion rather than compensation, but in people who perform well it appears to be a genuine adaptation.

A related idea is cognitive reserve. This is the observation, supported by many studies, that people with more education, more demanding occupations or richer social lives can tolerate more brain damage before symptoms appear. Reserve is usually inferred rather than measured: it helps to explain why two people found after death to have similar amounts of plaque and tangle in their brains can have differed markedly in how well they functioned. It may also explain why some people remain mentally sharp into their nineties while others decline early.

Researchers have also identified factors that seem to protect the brain. A widely cited trial published in 2011 put older adults through a year of moderate aerobic exercise and reported a small increase in the size of the hippocampus, a result that surprised many specialists. Physical activity, the control of blood pressure and other aspects of vascular health appear repeatedly in large studies: what is good for the heart seems to be good for the brain. A major review of dementia prevention published in 2020 listed hearing loss, hypertension and physical inactivity among the factors that people can act on, though it stressed that none of them guarantees protection.

Much remains uncertain. Adult neurogenesis, the birth of new neurons in the adult hippocampus, is well established in rodents, but whether it occurs on a meaningful scale in humans is still debated, with studies of human tissue producing contradictory results. Why some brains age faster than others is equally unexplained. Some people in their nineties perform as well as people decades younger, and post-mortem studies suggest that their brains contain fewer of the deposits associated with disease. Nor is it clear how far the changes seen on scans translate into the difficulties people actually experience in daily life.

What is clear is that ageing is not a single process that happens at the same rate everywhere. It is a collection of changes, some of which begin early and some late, some of which matter a great deal and some hardly at all. Understanding that variety is the first step towards distinguishing ordinary ageing from the diseases that can be treated.

In the early 1990s, a blood test became available that could tell people whether they carried the mutation responsible for Huntington's disease. The illness is inherited in a straightforward way: a child of an affected parent has a fifty per cent chance of carrying the mutation, and those who do will almost certainly develop the disease, usually in middle age. There is no cure. The test therefore does something unusual in medicine: it neither diagnoses an illness that is already present nor offers a route to prevention. It tells a healthy person what is likely to happen to them, years or decades in advance. Since then, similar questions have arisen about tests for other conditions, including inherited forms of cancer and, more controversially, the common forms of Alzheimer's disease.

The argument for offering such information rests on autonomy. Medicine has largely abandoned the habit of withholding bad news from patients, and few people now accept that a doctor should decide what a competent adult can bear to know. Knowing one's status can be useful in practical ways: it allows a person to plan financially, to decide whether to have children and to consider whether to be tested for other conditions. It can also end years of uncertainty, which many people find harder to endure than a definite answer, even a bleak one. The alternative to testing, after all, is not blissful ignorance but a vague and persistent dread, since anyone with an affected parent already knows the odds.

Against this stands the old fear that the news will do harm. A person told that they will develop a fatal illness may become depressed, anxious or even suicidal; they may give up work, or interpret every stumble as the first sign. There is also the principle, recognised in medical ethics, of the right not to know. A patient who suspects that they carry the mutation may reasonably decide that a definite answer would make their remaining healthy years worse rather than better, and no one else is entitled to make that choice for them. The fear behind this principle is not irrational, because a result cannot be unknown once it has been given.

A different objection concerns accuracy. A risk figure derived from a genetic test describes a population, not a person. This is particularly true of the tests now offered for Alzheimer's disease. The best known genetic risk factor, a variant of the gene APOE known as APOE4, raises the likelihood of developing the illness, but plenty of people who carry it never develop dementia, and plenty who do not carry it develop the disease anyway. The polygenic risk scores sold by some companies, which combine many small genetic effects into a single number, are harder to interpret still. A commercial test that reports a raised risk may be statistically defensible and personally meaningless at the same time.

Then there are the consequences that follow a result. In most countries insurers may ask about family history, and in some they may take account of genetic results above certain policy values; a voluntary agreement in the United Kingdom restricts their use. Employment is a further concern, since a person known to be at high risk may be passed over for promotion or refused a job. Neither outcome has anything to do with medicine, yet both flow directly from the decision to be tested, and both fall most heavily on people who are already unwell or poorly paid. Legislation differs sharply from one country to another, which means that the same result can carry very different consequences depending on where a person lives.

The evidence from clinics is more reassuring than the warnings suggest. Predictive testing programmes generally require several counselling sessions before a sample is taken. A waiting period then follows, giving the patient time for reflection. Reviews of these programmes have found that serious psychological harm is less common than was feared, and that most people who receive a positive result cope better than they had expected. A minority experience lasting distress, and it is not always possible to predict who they will be. This does not mean that counselling is unnecessary; it means that its purpose is to prepare people for information rather than to protect them from it.

This is why the middle path seems right. Testing should be offered, with counselling and time, rather than promoted. The problem with much direct-to-consumer advertising is not that it exists but that it presents risk as though it were diagnosis, offering a certainty that the science cannot supply. Where companies sell tests for conditions that have no treatment, and where no counselling is provided, the balance of benefit and harm shifts against the customer. Regulation, rather than prohibition, is the appropriate response, since a ban would remove a service that many people want and some genuinely need.

So people should be told their risk — but only if they have asked, only with the support that makes the information usable, and only when the figure means what it appears to mean. The question is not whether knowledge is good in general, but whether this knowledge, given in this way, to this person, is good. That is a question medicine can answer only case by case, and a blanket rule either way would serve neither the cautious nor the curious.