Frequently asked questions

Alzheimer’s disease always follows a slowly progressive course of up to 20 years, with an average of around 10 or 12 years. Although it is artificial, the evolution of symptoms is usually divided into three phases.

In the first (mild) phase, the first symptoms are related to memory loss. The person begins to have trouble remembering recent events. Repeat questions or actions repeatedly. They forget important dates and the names of people they know, or they lose personal objects at home because they can’t remember where they were stored.

The first failures appear in the temporal orientation (confuses the day in which he lives) or spatial (he makes a mistake when choosing a street address or does not know how to find the way to some perfectly known place). The person begins to experience language difficulties as either an expressive or understanding disorder. It usually begins with a difficulty in naming words (anomie) that progressively advances. Habitual words remain on the tip of the tongue, without coming out, he needs to make detours to express what he wants to say.

Difficulties arise in manipulating objects, gesticulating and carrying out coordinated movements for a specific purpose. In the same manner, the alteration of the executive functions becomes evident by the progressive decrease of multiple skills necessary for the performance of activities in daily life such as the capacity for judgment, planning, reasoning, abstraction or organization of tasks, which entails a loss of the capacity for performing the most complex tasks in daily life, the so-called complex instrumental activities, such as those required to carry out social or working activities and to achieve new cognitive learning.

In the second (moderate) phase, cognitive changes become much more evident and debilitating for the person who suffers from these changes. Memory failures for recent events are very evident, although the person continues to remember relatively well the events of the past and mentions them continuously in conversations with others. Language becomes increasingly difficult, does not find words, confuses words with each other, and often does not understand well what is said. The patient gets lost in familiar places or even in his own home. Little by little he loses the notion of the passage of time. In addition, he has difficulties in recognizing familiar objects, places or people; he may even stop recognizing himself.

Delirious symptoms and hallucinations may appear, such as believing that they are being robbed, persecuted or that their spouse is unfaithful. They have difficulty using simple objects, such as cutlery at mealtime, and have great difficulty doing their own cleaning or dressing on a daily basis. They lose the ability to make decisions, solve problems, and it is difficult to reason with them. It is becomes increasingly difficult to carry out instrumental activities such as shopping, managing money or maintaining an adequate diet.

In the third (severe) phase, the patient hardly retains any cognitive capacity. The ability to communicate through language is lost. Incontinence of sphincters appears and the progressive loss of the ability to walk. The patient has less and less appetite and refuses to eat. At times he is agitated or even aggressive physically or verbally and may have difficulty falling or staying asleep. They are completely dependent on their caregivers, even for the most basic care.

Alzheimer’s appears very rarely in heredity. Only 1% of all cases have a family inheritance, with at least one of the affected parents. In these cases, the disease will appear at a young age, below the age of 60. In the remaining 99%, the disease usually appears from the age of 65 and, although its final cause is unknown, it will have a multifactorial origin that includes toxins, environmental factors, lifestyle factors and the influence of some risk genes.

The cause of Alzheimer’s disease is still unknown. Although we know the neurodegenerative processes that take place in the patient’s brain, we do not know the factors that trigger neurodegeneration. Only 1% of cases are caused by genetic alteration.

The diagnosis of Alzheimer’s disease is fundamentally clinical and is established as a probability in the life of the patient. The definitive certainty diagnosis can only be established with the pathological study of the postmortem brain when the presence in the brain of a series of pathological changes is demonstrated, which in a generic way consist of cerebral atrophy, loss of neurons and deposits of abnormal proteins inside and outside the neurons. On the outside of the cells, the beta-amyloid protein (Aβ) is deposited in the form of plaques called senile plaques and on the inside, the tau protein is accumulated, which is called neurofibrillary tangles.

The clinical diagnosis is reliably confirmed in about 90% of cases. In order to verify that the subject meets the diagnostic criteria required to establish the diagnosis of Alzheimer’s disease, it will be necessary to carry out a specific diagnostic evaluation that includes a neuropsychological examination that demonstrates the existence of the cognitive disorders, at the same time as defining their characteristics and intensity. In addition, a comprehensive clinical case history of the patient, supplemented by data from a reliable informant, as well as a full neurological examination and complementary tests such as a blood test and neuroimaging demonstrating cerebral atrophy in a nuclear magnetic resonance (MRI), decreased cerebral blood flow in a single photon emission tomography (SPECT), or reduced cerebral cortex metabolism in positron emission tomography (PET) are required.

At present, the focus of diagnosis is on making it possible in the early stages of the disease. In this sense, it is known that cerebrospinal fluid (CSF) is the most important source of biomarkers for Alzheimer’s disease, having become in recent years a means for early diagnosis of the disease in which tau proteins stand out as more consistent and reliable, either their total levels (total tau) or their phosphorylated forms (phospho-tau) and the protein β-amyloid of 42 amino acids (βA1-42). The CSF of Alzheimer’s patients shows low levels of βA1-42 and high levels of total tau or phospho-tau. The greatest clinical utility is observed when both biomarkers are examined together through the ratio of βA1-42/tau whose elevation increases the sensitivity of the clinical diagnosis.

There is currently no treatment that can stop or change the course of the disease. However, in recent years, with the emergence of second generation acetylcholinesterase inhibitor (ACEI) drugs and later memantine, there has been encouraging progress in the treatment of Alzheimer’s disease. The aim is to maximise cognitive and functional status and minimise the presence of emotional and behavioural disorders, as well as to contribute to improving the quality of life of patients and their carers. However, its effectiveness is currently limited in time and intensity.

The currently available ACTIs are donepezil, rivastigmine and galantamine. They have shown modest efficacy in the treatment of mild or moderate Alzheimer’s cognitive impairment, as well as in the control of behavioural disorders. It is advisable to maintain its use if the disease improves, stabilises or if the rate of deterioration observed before treatment begins slows down, even in later stages of the disease, provided that its effectiveness and the absence of adverse effects are proven.

Memantine contributes to the reduction of pathologically elevated levels of glutamate observed in the disease, which may contribute to synaptic dysfunction and neuronal death. It is approved in our country for use from the moderate phase of the disease. In patients with moderate to severe dementia it has shown modest improvements in general cognition, functional ability and behavioural disorders.

Recently, the hypothesis that the combination of certain nutrients could provide clinically relevant benefits in Alzheimer’s patients has laid the groundwork for the development of foods with medicinal effect. The result of this research has been the appearance of Souvenaid, a multicomponent drink designed to improve the functioning of neuronal synapses. It contains the necessary precursors and supporting nutrients to act synergistically improving the formation and function of the neuronal membrane in Alzheimer’s patients.

There is also evidence in favour of the efficacy of non-pharmacological approaches in the treatment of Alzheimer’s disease. Cognitive Intervention Therapies (ICT) and Occupational Therapy are therapeutic strategies based on brain neuroplasticity and based on cognitive neuropsychology and behaviour modification therapies aimed at favouring the operative functionality of the patient and maintaining his autonomy. ICT involves the guided practice of a set of tasks designed to stimulate or particularly train cognitive functions such as memory, attention or executive skills, which can be performed in a variety of formats and procedures.

ICTs have also demonstrated beneficial effects on the behavioural alterations of dementia, especially in the case of apathy, anxiety, irritability and depression, and should therefore be considered as a therapeutic option for addressing not only the deterioration of cognitive and functional capacities, but also behavioural manifestations in patients with mild or moderate Alzheimer’s disease.

It is a therapeutic program of integral cognitive stimulation that is based on the existence of neuronal plasticity and on the principles of cognitive neuropsychology and behavior therapy that tries to maintain cognitive functions, prevent and treat behavior problems and facilitate the performance of daily life activities by the patient. Its final objective is to conserve and improve the cognitive resources that the patient still conserves in the short and medium term through the practice of appropriate activities for this purpose.

The programme focuses on mild and moderate cognitive impairment and is conducted at all times under the direction and supervision of professionals specialised in cognitive stimulation in people with dementia. The program is designed in a personalized and structured way according to the personal characteristics of each person: level of cognitive impairment, educational level, social relations, interests, leisure activities, motivation…

The increase in successful experiences through integral cognitive stimulation helps to improve patients’ self-confidence and psychological well-being, reduces their psychological distress and consequently contributes to alleviating the burden and suffering of caregivers, improving both their quality of life and decreasing the likelihood of institutionalization of the patient.

In general, the Alzheimer’s patient should not drive, as this is a complex activity that requires quick decisions and reactions. Therefore, everyone with Alzheimer’s disease, as their disease progresses, will be prevented from driving because it will become a safety issue. It is known that the risk of suffering an accident is between 3 and 4 times greater for a driver with dementia than for another driver of the same age but who does not suffer cognitive deterioration.

Ideally, the Alzheimer’s patient’s family should get involved and convince them that the best thing for themselves and others is to get away from the wheel as soon as possible, standing firm so that they do not drive when it is no longer safe. In this sense, it is very important to take the person’s feelings into account when explaining why they should no longer drive, helping them make the decision while protecting their self-esteem.