Michael J. Fox’s Parkinson’s Disease Began Long Before the Tremor — and Now Science Can Detect It Earlier, Part 2

Fox spent many years trying to understand why he became ill at such a young age. He recalled head injuries, alcohol use, working and living in different places, and possible contact with chemicals. He said that he caught and ate fish from a river near pulp and paper plants, spent time on farms and may have come into contact with agricultural chemicals.

The environment and the mystery of Fox himself

In a 2023 CBS interview, Fox said that he considers some kind of chemical exposure the most likely explanation for himself, although he does not know exactly what it was. He expressed this idea with the phrase: genetics “loads the gun,” and the environment “pulls the trigger”.

Today, for some environmental exposures, the connection with Parkinson’s disease indeed appears more convincing than for others. The most consistently discussed are certain pesticides and herbicides, some industrial solvents, in particular trichloroethylene (TCE). But even here, we are talking about an increase in risk, not a direct formula of “was exposed - will become ill.”

Filming of the series Leo & Me

An especially mysterious episode remains the series “Leo & Me”, in which Fox acted as a teenager in Vancouver. It was later discovered that Parkinson’s disease developed in several other people who had worked on this series. Reports from the early 2000s mentioned four cases among approximately 125 members of the production team - an unusually high frequency for such a small group. Those affected included script supervisor Sally Gardner, director Don S. Williams and one of the camera operators whose name we do not know.

This is what interested neurologists: those affected performed different jobs, so if a common factor really existed, it was unlikely to have been related to one specific profession or one special effect. The possibility of a common toxic, infectious or other environmental exposure was discussed, but the specific source was never found. To this day, there is no evidence allowing this cluster to be linked to a particular chemical substance or another specific environmental exposure.

When I re-examined the history of this cluster, one interesting detail emerged. There is direct evidence that “Leo & Me” was filmed in Studio 40 at the CBC Vancouver center. Two years earlier, in 1976, the program “Let Us Remember” was filmed in the same Studio 40: trenches with wet soil were built inside and a large amount of water was used to create artificial rain. The studio was located on the lower, underground level of the complex. We do not know whether persistent dampness or mold developed afterward and exactly how the room was dried, but such large-scale water exposure in a large enclosed space with porous and sound-absorbing materials makes this history worthy of attention.

The question of shared ventilation is particularly interesting. Some of those who later developed the disease worked directly on the filming set, while Sally Gardner spent a significant portion of her time in the control room. If Studio 40 and the control room areas were connected by a shared air supply and return system or recirculation system, people located in different rooms could still have been exposed to the same factor. This still does not prove the cause of the Vancouver cluster, but it already represents a specific and testable direction for further investigation.

Mold and mycotoxins: where the data end and the hypothesis begins

Experimental studies have shown that some substances produced by molds are capable of affecting the same cellular processes that are disrupted in Parkinson’s disease. Of particular interest are mycotoxins capable of damaging cells of the dopamine system, increasing inflammation and affecting the metabolism of alpha-synuclein - a protein whose pathological accumulation plays an important role in Parkinson’s disease. At the same time, some of these substances can disrupt the cellular systems that normally remove damaged proteins. As a result, a potentially unfavorable combination arises: more pathological alpha-synuclein is produced, while the cell’s ability to eliminate it decreases.

Among the most studied substances in this context are ochratoxin A and aflatoxin B1. They can be produced by some species of molds, including representatives of the genera Aspergillus and Penicillium.

This is also important from the point of view of the environment. Such fungi are found not only in food products, but also in damp and water-damaged buildings. Their particles, contaminated dust and metabolic products can spread throughout a room, and with a shared ventilation system, exposure is potentially not limited to the room where the source itself is located.

Mold and Parkinson’s Disease: The Steve Locke Case

An interesting case received widespread attention in the United States in 2025. Steve Locke - a former CEO of USA Triathlon and multiple Ironman participant - began experiencing problems with his gait after moving into an apartment in Colorado Springs, and later developed tremor. In 2015, he was diagnosed with Parkinson’s disease. For several years, the family did not connect what was happening with their home.

It was not until 2020, after another leak, that the structures were opened and long-term water damage, mold, and deterioration of materials inside the walls, ceilings, and floors were discovered. The family stated that the exposure had continued for several years and could have been related to the deterioration in the health of everyone living in the apartment.

The story of their son is particularly interesting. Several months after Locke developed his first symptoms, their five-year-old child suddenly developed motor and vocal tics. His mother also reported that all three family members were later found to have abnormalities that she described as immune dysfunction. Tics can occur in PANS, but based on the published description it is not possible to make this diagnosis in the child: PANS requires, first of all, the sudden onset of severe OCD or markedly restricted food intake together with other acutely developing neuropsychiatric symptoms.

In 2022, the family filed a lawsuit against the property owner and management company, claiming that long-term mold exposure played a causal role in the development of Parkinson’s disease in Steve Locke. The case was scheduled to go before a jury in February 2025, but three days before the trial was due to begin, the parties reached a settlement. Therefore, no court decision was issued establishing a causal relationship between mold exposure and Parkinson’s disease.

This story is particularly interesting in light of experimental data. One of the fungal substances being studied is 1-octen-3-ol - a volatile organic compound released by some fungi and involved in the characteristic smell of mold. In laboratory studies, it reduced dopamine levels, disrupted its normal transport within nerve cells, damaged dopaminergic neurons - the very cells that are particularly affected in Parkinson’s disease, and produced Parkinson-like motor abnormalities in laboratory organisms.

The Steve Locke case does not prove that living in a mold-contaminated building causes Parkinson’s disease in humans. But it brings together several observations that deserve further study: long-term exposure in a water-damaged building, the development of Parkinson’s disease in an adult, sudden neurological symptoms in a child from the same family, and experimental evidence that some fungal substances can damage the dopaminergic system.

PPMI: from the search for progression markers to personalized medicine

The foundation created by Michael Fox had an even greater influence not on the treatment of existing symptoms, but on the very understanding of the disease. In 2010, it launched the Parkinson’s Progression Markers Initiative (PPMI) - an initiative to study markers of Parkinson’s disease progression - a large international study whose participants undergo examinations for years, have brain imaging and provide samples of blood, cerebrospinal fluid and other biological materials. Researchers wanted to trace how the disease begins and changes over time and whether its biological signs can be detected before the usual motor symptoms appear. PPMI data were made available to researchers around the world, and the project gradually turned into a huge international scientific platform. Today, more than 50,000 volunteers provide data online, and more than 5,000 undergo detailed examinations at 50 medical centers in 12 countries.

One of the most important results of this work was the confirmation of a new method for detecting pathologically altered alpha-synuclein - a protein that plays a central role in Parkinson’s disease. This represented a fundamental change in approach: the disease began to be sought not only by how a person moves, but also by what is already happening in the body. We will return to this again later.

In 2026, PPMI retained the same abbreviation, but received a new name - Parkinson’s Precision Medicine Initiative, an initiative for precision medicine in Parkinson’s disease. It reflects the next stage of research: the task now is not only to detect the disease earlier, but also to understand its biological differences in different patients and in the future to select treatment taking into account the biological characteristics of a specific patient and the stage of the disease.

Over a quarter of a century, The Michael J. Fox Foundation has helped attract and direct more than $3 billion toward Parkinson’s disease research. But perhaps the most important result of its work is measured not only in money and not in the number of funded projects. The question that grew out of the personal history of one actor gradually became one of the central questions of modern Parkinson’s disease science: what was happening in the nervous system before the little finger began to move - and can the disease be detected early enough to have time to change its course before pronounced symptoms appear?

The Fox Foundation breakthrough: the disease can be sought before tremor appears

One of the most important results of PPMI was the testing of a new method - the αSyn-SAA assay, which makes it possible to detect pathologically altered alpha-synuclein. An ordinary test might simply measure how much alpha-synuclein is present in a sample. αSyn-SAA works differently: it looks for the pathological form of the protein that is able to trigger incorrect folding of other alpha-synuclein molecules. In the laboratory, conditions are created in which this process is repeated and amplified many times until the signal becomes measurable. In this way, it is possible to detect a very small amount of pathologically altered alpha-synuclein in cerebrospinal fluid - the fluid surrounding the brain and spinal cord.

Most importantly - pathological alpha-synuclein is found not only in patients with already noticeable disease. In some people from higher-risk groups, the test becomes positive before the usual clinical diagnosis.

At the same time, αSyn-SAA is not simply a “Parkinson’s test.” In some patients with clinically confirmed disease, the test may remain negative. In addition, pathologically altered alpha-synuclein accumulates not only in Parkinson’s disease, but also in other diseases of the nervous system, including dementia with Lewy bodies and multiple system atrophy. The ability of αSyn-SAA to detect these diseases differs and depends on the methodology used. Pathological alpha-synuclein may also be detected in people with isolated REM sleep behavior disorder or pure autonomic failure before the classical picture of Parkinson’s disease or another neurodegenerative disease appears. Therefore, a positive αSyn-SAA result indicates the presence of a pathological process associated with alpha-synuclein, but by itself does not establish a diagnosis of Parkinson’s disease.

But for the prevention and study of Parkinson’s disease, the significance of this discovery is enormous. It is now possible to select for research people in whom the disease has not yet manifested with the usual tremor or stiffness, but whose biological signs are already detectable.

Can you calculate your own risk of Parkinson’s disease?

For evaluating the very early, prodromal stage of Parkinson’s disease, there is a special system developed by the International Parkinson and Movement Disorder Society. It takes into account a person’s age, symptoms, examination results, family history and some other factors. First, the baseline probability for a particular age is determined, and then each additional sign changes that probability.

To show how important each sign is, a measure called LR is used. The easiest way to think of it is as the “weight” of a sign: the higher the LR, the greater the importance of that sign in the overall assessment.

At the same time, LR is not a percentage of risk. It is a way to show how strongly a particular sign influences the final assessment compared with other signs. The baseline probability directly depends on age. In this model, it is approximately 0.4% at age 50–54, 1.25% at 60–64, 2% at 65–69, 2.5% at 70–74, 3.5% at 75–79 and about 4% after age 80.

But it is much more interesting to see how different the “weight” of individual signs can be:

Factor or sign	Its weight in the overall assessment, LR
REM sleep behavior disorder confirmed by sleep study	130
Pronounced changes on imaging of the brain’s dopamine system	43.3
Drop in blood pressure on standing due to impaired nervous regulation of vessels	18.5
First signs of parkinsonism on neurological examination	9.6
Objectively confirmed loss of smell	6.4
Changes on specialized quantitative movement testing	3.5
Erectile dysfunction in men	3.4
Symptomatic drop in blood pressure on standing	3.2
Possible REM sleep behavior disorder based only on questionnaire	2.8
Pronounced daytime sleepiness	2.7
Parkinson’s disease in a close relative	2.5
Constipation	2.5
Urinary disturbances	2.0
Pronounced memory and thinking impairment	1.8
Depression or anxiety	1.6
Regular contact with pesticides	1.5
Occupational contact with solvents	1.5
Type 2 diabetes	1.5
Low physical activity	1.3
Male sex	1.2

This table clearly shows why you cannot simply count the number of “early symptoms.” For example, constipation really can appear long before the motor symptoms of Parkinson’s disease. But its weight is only 2.5 because constipation is very common even in completely healthy people.

REM sleep behavior disorder confirmed by a sleep study has a completely different significance. With this disorder, a person begins to move, talk, wave their arms or physically participate in what is happening in the dream during vivid dreams. The weight of this sign in the model is 130.

This system is not intended for a person to diagnose themselves using a table. Its purpose is different: to help specialists assess how closely the combination of existing signs resembles a very early stage of Parkinson’s disease and who may particularly benefit from further examination and observation. At the same time, it can help a person better understand their own level of risk if they assess their existing symptoms and risk factors, but such an assessment does not replace medical diagnosis.

What can be tested today?

Even when suspicious early signs are present, Parkinson’s disease is still not diagnosed with a single test. The physician begins with a neurological examination: assessing speed of movement, muscle stiffness, tremor, gait, arm movements while walking, symmetry of the right and left sides and the ability to perform rapid repetitive finger movements. If there is suspicion of REM sleep behavior disorder, in which a person may move, talk or act out dream content, a sleep study is performed.

With reduced sense of smell, a standardized test can be used to objectively determine whether the ability to distinguish odors is actually reduced. Such a free smell test can be ordered through The Michael J. Fox Foundation’s PPMI program. In the United States and Canada, it is offered to people with diagnosed Parkinson’s disease, as well as to people aged 60 and older without this diagnosis - to assess reduced sense of smell as one of the possible early risk factors. The test is mailed to the home, the person completes it independently and enters the results online. The foundation uses this assessment in studies of early signs and risk of Parkinson’s disease.

With very early onset of the disease or a strong family history, genetic testing may be useful. At the same time, an ordinary commercial genetic test checking one or two known variants does not replace an expanded panel that includes more than 80 genes associated with inherited forms of Parkinson’s disease and other movement disorders.

There is also DAT-SPECT - a special scan that makes it possible to assess the condition of nerve endings in the brain’s dopamine system. It can be useful if the physician is uncertain whether a movement disorder is related to degeneration of this system. But the study does not show the cause of the disease and by itself does not establish a diagnosis of Parkinson’s disease.

New methods also make it possible to look for pathological alpha-synuclein. In addition to αSyn-SAA in cerebrospinal fluid, there is testing of small skin samples. Pathologically altered alpha-synuclein is also sought in nerve fibers in the skin. A positive result, as discussed earlier, indicates a disease from the group of synucleinopathies - diseases in which this protein pathologically accumulates in the nervous system, - but does not prove Parkinson’s disease specifically, because similar changes also occur in some other neurodegenerative diseases.

Measuring dopamine in blood or urine does not show how well the brain’s dopamine system is functioning. For the same reason, urine tests for HVA and commercial “neurotransmitter panels” are not used to diagnose Parkinson’s disease.

Prognosis and Life Expectancy

Parkinson’s disease progresses at very different rates in different people. With early-onset disease, a person may live with the diagnosis for decades. These patients often preserve memory and the ability to manage daily activities independently for longer, although over many years they are more likely to experience increasingly uneven medication effects and involuntary movements. Michael Fox is a clear example: he was diagnosed at about age 29, and he is now 65 - about 35 years with the disease.

With modern treatment, life expectancy in many patients may be close to that of people without Parkinson’s disease. Prognosis depends less on the severity of tremor than on age, memory and cognitive function, the ability to move independently, frequency of falls, autonomic nervous system function, swallowing function, and other medical conditions.

Parkinson’s disease can impair the automatic regulation of the heart and blood vessels. The disease affects not only the areas of the brain responsible for movement, but also the autonomic nervous system - the system that regulates heart rate, blood pressure, and vascular tone without conscious control.

Normally, when a person stands up, some blood shifts into the legs under the influence of gravity. The body immediately compensates: blood vessels constrict, and the heart begins to beat slightly faster and more forcefully so that blood pressure does not fall and the brain continues to receive enough blood.

In Parkinson’s disease, this compensatory system can become impaired. Sympathetic nerve endings that transmit signals to the heart may gradually be lost, and the baroreflex - the automatic mechanism that responds to changes in blood pressure - may also become impaired. As a result, when a person stands up, the blood vessels may not constrict enough, and the heart may not sufficiently increase its rate and force of contraction.

This can result in neurogenic orthostatic hypotension: a significant drop in blood pressure after moving into an upright position. A person may experience weakness, dizziness, darkening of vision, unsteadiness, or loss of consciousness. Sometimes a substantial drop in blood pressure occurs with almost no warning symptoms.

The main danger of this problem is reduced blood flow to the brain and the resulting risk of fainting, falls, and fractures. An impaired cardiac response to physical activity may also present as rapid fatigue and poor exercise tolerance.

At the same time, the problem is not always limited to low blood pressure. In the same patient, blood pressure may fall when standing or after meals but become too high while lying down or during the night. This happens because the system responsible for automatically regulating blood pressure itself has become impaired. A person may therefore have blood pressure that is too low under some conditions and too high under others.

This combination creates a double risk: low blood pressure increases the likelihood of fainting, falls, and injuries, while persistently elevated blood pressure when lying down may increase the burden on the heart, blood vessels, kidneys, and brain. Therefore, the cardiovascular problem in Parkinson’s disease is primarily not that the disease directly damages the heart muscle, but that the heart and blood vessels gradually lose part of their normal nervous control and become less able to adapt to changes in body position, food intake, and physical activity.

One of the most serious complications of the later stages remains impaired swallowing. Food, liquid, or saliva may enter the airways and cause aspiration pneumonia. Silent aspiration is particularly dangerous, because the person may have little or no cough when this happens. Swallowing impairment can also lead to weight loss, inadequate nutrition, and dehydration.

Falls and fractures are also important. They may result from several features of the disease at the same time - impaired balance, sudden “freezing” while walking, delayed protective movements, and a drop in blood pressure when standing. A fracture and the resulting period of immobility can trigger further decline: the person loses muscle strength more rapidly, becomes less independent, and becomes less able to tolerate subsequent illnesses.

Another important group of complications is infections. In addition to pneumonia, patients with significant autonomic dysfunction may develop impaired bladder emptying, which increases the risk of urinary tract infections. In an older person with Parkinson’s disease, an infection may sometimes present not so much with fever or pain, but with a sudden increase in weakness, confusion, worsening of walking, and a sharp increase in falls. A severe infection can lead to sepsis.

Thus, the main risks in the later stages are not related to the tremor itself. Prognosis is affected much more strongly by aspiration and pneumonia, impaired autonomic regulation of the heart and blood vessels, falls and fractures, infections, loss of mobility, inadequate nutrition and dehydration, as well as significant cognitive changes. For this reason, the care of a person with Parkinson’s disease eventually needs to extend far beyond controlling tremor and adjusting the dose of levodopa.

Cognitive Changes and Dementia

With Parkinson’s disease, problems with attention, speed of thinking, planning and visuospatial perception may appear over time, but dementia does not develop in every patient. If pronounced cognitive impairment develops after several years of established Parkinson’s disease and begins to noticeably interfere with everyday independence, the term Parkinson’s disease dementia is used.

There is also a closely related condition - dementia with Lewy bodies. In this condition, problems with thinking and memory appear before motor symptoms or at approximately the same time. For clinical distinction, the conventional one-year rule is traditionally used: if dementia develops more than one year after the onset of parkinsonism, it is called Parkinson’s disease dementia; if it begins earlier or within the first year, it is called dementia with Lewy bodies. This distinction is largely conventional because both conditions are associated with pathological accumulation of alpha-synuclein and share many features.

Unlike the typical picture of Alzheimer’s disease, in the early stages the more noticeable problems may be not so much difficulty remembering new information as fluctuations in attention, slowed thinking, difficulties with planning and spatial orientation. Vivid visual hallucinations and marked fluctuations in clarity of thinking during the day may also occur.

What if the disease has already been diagnosed?

Modern treatment of Parkinson’s disease can significantly reduce symptoms and help a person remain independent for longer. But it is fundamentally important to distinguish between symptom control and an effect on the disease itself. At present, there is no treatment proven to stop or reverse the ongoing damage to nerve cells. This is why, even with access to modern therapy, the disease may progress over time - Michael J. Fox’s story shows this well.

Medication therapy

The most effective medication for motor symptoms remains levodopa. In the body, it is converted into dopamine and partially compensates for its deficiency in the brain. It is usually prescribed together with carbidopa, which helps more of the levodopa reach the brain and reduces some side effects.

In addition to levodopa, other groups of medications are used. Dopamine agonists, such as pramipexole, ropinirole and rotigotine, imitate the action of dopamine. MAO-B inhibitors, such as rasagiline, selegiline and safinamide, slow the breakdown of dopamine and may be used both for milder early symptoms and together with levodopa. COMT inhibitors, such as entacapone, prolong the effect of levodopa when its effect no longer lasts until the next dose. Amantadine is more often used to reduce dyskinesias - excessive involuntary movements.

As the disease progresses, the treatment regimen often becomes more complex: doses and timing are changed, medications from different groups are combined, and the goal of therapy increasingly becomes making symptom control more even throughout the day.

Surgical methods

If medications no longer provide sufficiently stable control of motor symptoms, deep brain stimulation may help some patients. During the operation, electrodes are implanted into certain areas of the brain, through which weak electrical impulses are delivered. Such therapy can substantially reduce tremor, stiffness, slowing of movements, dyskinesias and periods of reduced medication effect.

However, deep brain stimulation also does not stop the disease itself and is not suitable for all patients. It works better for symptoms that previously responded well to levodopa, while balance problems, falls, changes in speech, memory and some other manifestations may continue to worsen over time.

Physical activity and rehabilitation

Physical activity has a very important place. Modern recommendations are oriented toward approximately 150 minutes of moderate- or high-intensity physical activity per week. It is desirable to combine aerobic exercise, strength training, stretching, balance and coordination training. For a person with Parkinson’s disease, movement is a full part of treatment, helping preserve gait, balance and the ability to independently perform daily activities for longer.

Rehabilitation is no less important. A physiotherapist works on gait, balance and fall prevention. An occupational therapist helps adapt daily activities and the environment so that the person can remain independent for longer. A speech and swallowing specialist helps with a quiet voice, changes in speech and swallowing impairment.

Swallowing impairment may begin unnoticed: a person eats more slowly, swallows one bite several times, feels that pills get stuck, or coughs after drinking water. Silent aspiration is especially dangerous - food, liquid or saliva entering the airways without obvious coughing. Therefore, when swallowing impairment is suspected, special studies are performed and rehabilitation is started if necessary.

Modern therapy can significantly improve quality of life and preserve function for many years, but so far it does not solve the main problem – it does not stop the neurodegenerative process itself.

Can the risk of Parkinson’s disease be reduced?

Some risk factors for Parkinson’s disease cannot be changed - above all age, heredity and genetic predisposition. But there are also exposures that can be reduced. If we use Fox’s own metaphor, genetics can “load the gun,” and the environment can “pull the trigger.” That is why prevention is primarily connected with those factors that a person can actually control.

Pesticides and herbicides are among the most studied environmental factors associated with Parkinson’s disease. Contact with them is possible not only in agriculture, but also when treating gardens and lawns, spraying areas, living near intensively treated fields and regularly spending time in places where lawn-care chemicals are actively used, including golf courses. Therefore, it is reasonable to avoid being nearby during spraying, use protection when working with such products yourself and, when possible, reduce their household use. Choosing organic foods also makes it possible to reduce intake of a number of pesticides through food.

Head injuries are another factor that can be partially controlled. Prevention of repeated injuries is especially important: a high-quality properly fitted helmet when riding a bicycle, scooter, skiing, skating and during other activities with a risk of falling, protective equipment during sports and work, and seat belts in a car.

Regular physical activity is associated with a lower risk of Parkinson’s disease. It is optimal to combine aerobic exercise, strength training, balance and coordination training. At the same time, it makes sense to monitor metabolic health: type 2 diabetes, blood glucose levels, blood pressure and other metabolic factors.

The nutritional status of the nervous system also matters. In studies, patients with Parkinson’s disease more often have lower levels of vitamin D and B12, disturbances in folate metabolism and higher homocysteine. A deficiency of B12 and folate can contribute to increased homocysteine, which is also associated with increased cardiovascular risk. In addition, its level may increase during treatment with levodopa.

Of particular interest is production of glutathione. Glutathione is one of the main intracellular antioxidants protecting cells from oxidative damage. Its level is reduced in the substantia nigra of the brain in Parkinson’s disease. Both glutathione itself and substances needed for its formation, including NAC (N-acetylcysteine), are being studied. A complete diet rich in natural antioxidants, including vitamin E, is also of great importance.

Finally, it is worth reducing exposure to industrial solvents, chemical pollutants and chronically contaminated environments - not only at work, but also in one’s own home. This also applies to prolonged time spent in damp or water-damaged buildings, especially if the source of contamination persists for months or years.

Particular attention should be paid to the environment in which a person spends the night: during sleep, the processes of recovery and removal of metabolic waste from the nervous system are especially active, so constant exposure to polluted air, volatile chemicals or contamination associated with mold growth in the bedroom is undesirable. With occupational exposure, good ventilation and appropriate protection from toxic substances are also necessary.

Conclusion

Parkinson’s disease probably begins long before the first tremor appears. By the time noticeable motor symptoms arise, the pathological process may already have been developing for many years. That is why the main shift in recent years has been the attempt to see the disease earlier - through a combination of prodromal signs, objective changes and biomarkers, including pathologically altered alpha-synuclein.

At the same time, it is becoming increasingly clear that in most people the disease cannot be explained by a single cause. Age, inherited vulnerability, features of mitochondrial function and systems for removing damaged proteins, previous inflammatory processes, injuries and environmental exposures can combine in different ways. The same exposure may therefore have almost no effect on one person and become a significant part of the pathological process in another.

The practical meaning of these changes in the understanding of Parkinson’s disease is that medicine is gradually shifting from treating already pronounced symptoms toward earlier identification of people at increased risk. The next task is to learn to determine exactly which processes have already begun in a particular person, which potentially modifiable factors continue to affect them, and whether it is possible to intervene early enough while a significant part of the nervous system is still preserved.