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Les troubles de l'esprit

Depression and Manic Depression

Anxiety Disorders

Alzheimer’s- type Dementia

Help Link : Affections connexes Link : Alzheimer's Society UK Link : Autres maladies neurodégénératives
Link : Introduction à la maladie d’Alzheimer Link : Les démences Link : La démence: définition et signes prédictifs
Original modules
Experiment Module: Prospective Treatments for Alzheimer’s Disease Prospective Treatments for Alzheimer’s
  Experiment Module: The Effects of Normal Aging on Our Cognitive Abilities   The Effects of Normal Aging on Our Cognitive Abilities
History Module: Dr. Alois Alzheimer's First Cases   Dr. Alois Alzheimer’s First Cases

Free Radicals and Aging: More Complicated Than We Thought

Donating Your Brain to Science

According to Dr. Judes Poirier, a specialist in aging, the state of the brain of someone with Alzheimer’s-type dementia is comparable to that of the brain of a healthy person whose brain has aged normally but who has lived to be 150 or 160 years old!

According to Dr. Poirier, “From age 30 or 40 on, we lose an average of 4 to 10% of our neurons every 10 years. If we were lucky enough to live to age 150 or 160, we would almost certainly all have Alzheimer’s disease. And also Parkinson’s disease, because from a biological standpoint, if we lose 70% to 80% of the neurons in the parts of the brain involved in movement, we develop Parkinson’s disease, and if we lose 70% to 80% of the neurons in the parts of the brain involved in memory, we develop Alzheimer’s.

"[...] Because we do not actually live that long, Alzheimer’s disease may be described as a very accelerated form of aging, in which the effects emerge at age 60 or 65 rather than 150 or 160."

Link : Quelle différence y a-t-il entre le vieillissement normal et la maladie d’Alzheimer? Link : La maladie de Parkinson

There are more than 50 different kinds of dementia, and their causes are highly varied. Here are brief descriptions of some of the most common ones besides Alzheimer’s.

Vascular dementia is often said to account for about 20% of all cases of dementia. It occurs following strokes, which can vary in their number and severity. The location of the lesions varies as well; it can be cortical, sub-cortical, or both. Vascular dementia often occurs together with Alzheimer’s-type dementia, in which case the person is said to have mixed dementia.

Frontotemporal dementia is caused by Pick’s disease or by frontal-lobe deterioration of other origin. If the most affected part of the brain is the orbitofrontal lobe, then one of the most common symptoms is a tendency toward disinhibition. If it is the dorsolateral frontal lobe, then the more predominant symptom is apathy. In both cases, unlike in Alzheimer’s-type dementia, episodic memory is preserved for a long time.

Lewy body dementia is hard to diagnose, because it presents in a form that is midway between Alzheimer’s and Parkinson’s diseases. Moreover, it also has a number of symptoms in common with vascular dementia—visual hallucinations, for example.

Some kinds of dementia are reversible; those caused by a toxic reaction to medication are the most common type in this category. Other toxic substances, such as alcohol, heavy metals, and various street drugs, can cause such dementias, as can dietary deficiencies, infections, inflammations, tumours, hormonal disorders, and other causes.

Link : La démence et ses causes Link : Alzheimer

The brain, like the rest of the human body, changes throughout a person’s lifetime. After the brain’s rapid, spectacular development in the earliest years of life, its plasticity decreases and the changes slow, but they continue for as long as a person is alive. As people age, however, it is not unusual for them to experience a gradual decline in their intellectual faculties, and in particular their memory.

This is a natural phenomenon associated with normal aging of the brain (follow the Tool Module link to the left). But in some people, this decline happens much faster, with disastrous consequences in their lives and the lives of their families.

The general term for this phenomenon, dementia, was first used in the early 19th century. At that time, dementia was regarded as a form of what was called “mental alienation”, which also included schizophrenia and mood swings. And because the most serious symptoms were most often seen in elderly people, the expression “senile dementia” also came into use (it is now used less and less).  

Today, various types of dementia are distinguished (see second sidebar), but all have a common definition that, on the basis of World Health Organization diagnostic criteria, may be stated as follows: “a gradual loss of memory and of the ability to form and organize ideas, severe enough to interfere with activities of daily living, and present for at least six months”.

The cognitive and social problems associated with dementia result not from psychiatric disorders, but rather from organic causes that have been well characterized: specifically, an abnormally high number of neurons deteriorating and dying in certain parts of the brain. In this sense, the various forms of dementia are part of the broader category of neurodegenerative diseases (see box below).

This degenerative process disrupts the neurons’ communication function, thus causing many symptoms of dementia. These symptoms appear in adulthood and in most cases gradually worsen irreversibly.

Cognitively, individuals may experience memory problems. They may often repeat the same question, or buy the same thing twice. They may become disoriented, wandering around their own neighbourhood for hours, or lose their sense of time. They may become confused if they have to attempt tasks that require abstract planning, such as running errands or making transfers when travelling by public transit.

Linguistically, to compensate for having forgotten specific words, people with dementia tend to use catch-all terms like “thingy” or “gizmo”. They may also have problems in remembering important dates such as birthdays, or the names of famous people. Their motor skills may also be impaired when they try to operate familiar household appliances.

Emotionally, people with dementia may become sad, unstable, or even verbally or physically aggressive. They may act socially disinhibited and overfamiliar at some times, and fearful or suspicious at others, or they may experience episodes of euphoria, depression, or anxiety.

Behaviourally, people with dementia show less interest in other people, lose contact with their friends, and gradually give up their leisure pastimes. Often their movements become slower, which can, for example, make it hard for them to drive a car, or simply to comb their hair or brush their teeth. 

The best known form of dementia is Alzheimer’s-type dementia, commonly known as Alzheimer’s disease. It is also the most widespread form, accounting for 60 to 65% of all dementia cases.

Alzheimer’s-type dementia affects the brain only. And within the brain, it is the thin layer of grey matter, the cortex, that is affected. In this type of dementia, the first observable deficits begin in the hippocampus and the entorhinal cortex, two parts of the brain that are relatively old in evolutionary terms and that are involved in memory, so these deficits take the form of memory disorders.

Subsequently, other functions become impaired as well, such as language, orientation in time and space, the ability to plan activities, the ability to recognize faces and objects, and so on. People with Alzheimer’s-type dementia may also experience mood swings and become apathetic or depressed. At the severe stage of the disease, they become so confused and their movements become so laboured that they no longer have the skills needed to carry out their activities of daily living (washing, dressing, eating, and so on) on their own.

Though scientists do not yet know how to stop the progress of Alzheimer’s-type dementia, much less cure it, various medications and other treatments can relieve some symptoms and improve the quality of life of individuals who have it (follow the advanced Tool Module link to the left).

This is also an area in which a great deal of research is being done. Some studies have revealed two major degenerative processes that are associated with neuronal death. The traces that these two processes leave outside and inside the neurons were described for the first time by German physician Alois Alzheimer in 1906 (follow the beginner History Module link to the left).


The term neurodegenerative diseases designates a variety of pathologies that gradually result in the death of the neurons and the destruction of the nervous system.

Although some of these diseases occur in children and young adults, most of them occur in people over age 65. The resulting impairments may be predominantly cognitive, as in Alzheimer’s-type dementia, or predominantly motor, as in Parkinson’s disease, or a combination of the two, as in Huntington’s disease or Creutzfeldt-Jakob disease.

The various neurodegenerative diseases have certain similarities. In most cases, genetic factors that produce a hereditary form of the disease are known, but the disease also occurs in what is called a sporadic form, in people who have no family history of the disease. That does not, however, exclude the involvement of genetic factors.

The types of neurons and areas of the brain affected vary greatly from one neurodegenerative disease to another. The pyramidal neurons of the temporal cortex are heavily affected in Alzheimer’s-type dementia. In Parkinson’s disease, the dopamine-secreting neurons of the substantia nigra degenerate. In people with Huntington’s disease, the atrophy occurs in the striatum, the caudate nucleus, and the putamen. In people with amyotrophic lateral sclerosis, it occurs in the motor neurons of the cerebral cortex and the spinal cord. And in people with multiple sclerosis, it is the myelin sheath surrounding the axons of the central nervous system that is affected.

Link : Les maladies neuro-dégénératives Link : Maladies neurogégénératives Link : Neurodegeneration

Researchers have been trying for decades to discover a biological marker that would make it possible to distinguish Alzheimer’s from the normal aging process and from other neurodegenerative conditions (see box above). But we are still waiting for a simple blood test that would detect certain molecules indicating the presence of an Alzheimer’s-type dementia.

Hence a diagnosis of Alzheimer’s is still hard to make, among other reasons because the symptoms of Alzheimer’s can resemble benign memory loss or symptoms of other maladies such as depression. And even when Alzheimer’s is diagnosed, it is only a “likely” diagnosis, made by eliminating the other possible causes (a process known as differential diagnosis). The only way to to confirm a suspected case of Alzheimer’s is after the person’s death, by observing atrophy of the cortex together with two types of lesions that characterize Alzheimer’s: amyloid plaques and neurofibrillary tangles.

A physician’s first step in making a diagnosis will therefore be to question the patient and try to see whether he or she really has some form of dementia, by eliminating the other possible causes of dementia-like symptoms, such as a reaction to certain medications, a brain tumour, a stroke, a thyroid problem, or a chronic infection. The wide variations in the symptoms of Alzheimer’s make the diagnosis so uncertain that the physician will also question the patient’s family to try to better understand how his or her memory losses and other difficulties in daily living developed.

Next, the physician will use standardized tests, such as the Mini-Mental State Examination (MMSE), to assess the severity of the impairments of the patient’s various cognitive abilities, such as orientation in time and space and the abilities to memorize information, pay attention, or perform calculations. If necessary, the physician may also advise the patient to undergo a brain-imaging examination to increase the likelihood of an accurate diagnosis. Brain-imaging technologies unfortunately are not always accessible, because of their high cost, but they can, for example, be used to estimate the extent of cortical atrophy in various parts of the brain, the increase in the size of the cerebral ventricles, or the reduction in the metabolism of parts of the brain involved in memory. These techniques also make it possible to eliminate other causes, such as brain tumours, meningiomas, and multiple mini-strokes.

Tool Module: Brain Imaging Link : Obtenir un diagnostic Link : Steps to Diagnosis Link : MALADIE D’ALZHEIMER : va-t-on bientôt la prédire ? Link : Maladie d’Alzheimer : Un simple test sanguin pour diagnostiquer la maladie Link : Video : Dépister l'Alzheimer dans une simple goutte de sang Link : Les différentes lectures de la maladie d'Alzheimer

Link : Oxidative Stress Signaling in Alzheimer’s Disease Link : Alzheimer's disease : Causes Link : The cholinergic hypothesis of Alzheimer's disease: a review of progress Link : Oxidative Stress Signaling in Alzheimer’s Disease
Link : The cholinergic hypothesis of Alzheimer's disease: a review of progress
Original modules
Tool Module: Prospective Treatments for Alzheimer's Prospective Treatments for Alzheimer’s

Since the mid-1960s, a number of circumstantial links between aluminum and Alzheimer’s have been reported. It has therefore been hypothesized that this light metal, which is present not only in many objects that we use every day (such as cans, pots and pans, and various kitchen tools) but also in the air, ground, and water, might be one of the causes of Alzheimer’s.

But some of the studies that found the links in question have been criticized for faulty methodology, while others have been flatly contradicted by other research. For example, some critics think that in studies where linkages were found between aluminum and Alzheimer’s in lab animals, the doses of aluminum used were far too high compared with those to which humans are actually exposed. Moreover, it is very hard to measure the total amount of aluminum to which humans are exposed over a lifetime, because the sources of this metal in the environment are too numerous and too varied.

All of us are exposed to aluminum constantly, but in very small doses. For example, 99% of the aluminum that we ingest with our food is not absorbed by the digestive tract, and a large proportion of the remaining 1% is filtered out by our kidneys and excreted in our urine.

In other studies, the circumstantial link consisted in finding higher concentrations of aluminum in the brains of people with Alzheimer’s. But other researchers were unable to reproduce these findings. Also, researchers were unable to find some associations that they had expected. For example, they failed to find more cases of Alzheimer ’s in people who were exposed to aluminum in the workplace. They also failed to find any associations between Alzheimer’s and cultures that drink a lot of tea, even though tea is one of the plants that accumulates the most aluminum in its leaves.

Thus, despite the many studies that have been done on this subject, there is as yet no convincing evidence that aluminum is a risk factor for Alzheimer’s.

Link : Aluminium Link : Aluminium and Alzheimer's disease

For many diseases, the precise cause is known. For example, measles is caused by a virus, tuberculosis by a bacterium, and malaria by a protozoan.

But as with many other chronic conditions, there is no clearly identifiable cause of Alzheimer’s. Instead, the consensus is that this type of dementia develops under the influence of several factors. These risk factors may combine to overwhelm the natural mechanisms by which the brain repairs itself. A cascade of biochemical reactions then occurs, leading, years later, to the apperance of the earliest symptoms of Alzheimer’s. These risk factors are specific to each individual, but they can be divided into three main categories.

First, there are familial factors—the genes that we inherit from our parents. These factors can give members of certain families a predisposition to develop Alzheimer’s. In the rare “familial” form of Alzheimer’s, these genetic factors will have an even more direct effect.

The next category consists of environmental factors. For many decades, scientists believed that Alzheimer’s developed as the result of some environmental factor, such as a virus, a bacteria, or a toxic substance (in particular, aluminum—see sidebar). But one by one, these purely environmental hypotheses were discarded. Nonetheless, we do know today that the environment in the broad sense (diet, levels of stress, intellectual stimulation, physical exercise, and so on) does influence the development of Alzheimer’s. And for people with Alzheimer’s, a healthy, stimulating lifestyle gives them the best chance at a better quality of life.



Lasty, as we age, the interaction between our heredity and our environment leads to actual physiological disturbances in our bodies, such as chemical imbalances, immune deficiencies, an excess of toxic free radicals, and malformed proteins that disrupt the internal functioning of neurons or that become toxic by building up around them. Though none of these disturbances is the ultimate cause of Alzheimer’s, each of them leads to problems in neuronal communication that help to make it worse.

As so often happens in science, various hypotheses to try to explain the mechanisms behind Alzheimer’s have made one or the other of these disturbances their central focus. For example, the cholinergic hypothesis, which is one of the oldest, was the basis for most of the medications that have been developed to treat Alzheimer’s (follow the advanced Tool Module link to the left ). According to this hypothesis, Alzheimer’s is caused by insufficient synthesis of the neurotransmitter acetylcholine. But this hypothesis has become less popular, among other reasons because of the limited effectiveness of Alzheimer’s medications that attempt to compensate for acetylcholine deficiencies.

The amyloid hypothesis, first advanced in the early 1990s, is that deposits of amyloid plaques between the neurons are the primary cause of Alzheimer’s. This hypothesis is based, among other things, on the fact that type 4 of the apolipoprotein E gene, which is a recognized risk factor for Alzheimer’s, leads to overproduction of the amyloid fragment from which plaques form. This hypothesis continues to dominate much Alzheimer’s research, even though it has been subject to growing criticism.

The tau hypothesis has received increased suppport, especially since a study in 2004 showed that there were no clear correlations between deposits of amyloid plaques and loss of neurons. The name of this hypothesis refers to the name of a protein located in the neuron’s axon. In Alzheimer’s, this protein assumes abnormal forms, thus preventing the axon’s transportation system from working, impairing the neuron’s communication functions, and eventually causing it to die. According to the tau hypotheis, this cascade of events is the cause of Alzheimer’s.

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