Alzheimer: trend and resources Quebec

The trend in Quebec: keep the person with Alzheimer's at home and for as long as possible! Why: the federal and provincial governments believe that the cost of accommodation is high!

According to a study by the Institute of Geriatrics of Sherbrooke, even when institutionalization becomes possible, some families choose this option, but rather continue to treat the person at home ... Another study shows that caregivers who placed the patient home care experience less pleasure to heal than others who have not had recourse to institutionalization. Only until now unanimity among all participants: services (bathing, cleaning, meals on wheels, nurse, etc.). Are insufficient.

Maintaining home of the person with Alzheimer's disease

Human resources

The carer / employment of a person at home

The home help is the intervention of an employee who goes home for various tasks. (Cleaning, ironing, laundry, shopping, meal preparation and / or care for hygiene and grooming routine. ..)

This employee may be any person, except the spouse of the sick person.

His hiring may be done in three ways:

* The employee directly to the person (OTC)
* Through a public representative,
* Through a private service provider to the person,
* Or by an association.

The layout of the place of life

We should not hesitate to get help from competent people (social economy consultant and family therapists, social service assistants ...)

When planning a place to live, a few simple measures are recommended (not exhaustive):

* Prevent Accidents

The main danger lies in the kitchen and just gas.
The bathroom should be as functional and secure possible maximum temperature of the water blocked, soil anti-slip of handrails on the walls ...

* Prevent Falls: avoid unnecessary congestion, land sliding ...

* Promote autonomy in all parts of the house (easily accessible objects ...).

* Remove sources of stress and confusion:
o Do not move the familiar landmarks of the patient
o Promote the orientation of the person in time
+ Put a readable clock in every room
+ Hang an ephemeris (the person tear a page every day)
o Write legibly (eg over the telephone) the name, address and telephone number of the person.

Financing is possible with the ANAH (National Agency of habitat), the pension funds CNAVTS, and ARRCO IRCANTEC and the PALULOS (premium Improvement of rental housing and occupancy Sociale). Never start work before submitting the application for funding to these organizations.

Material aid

Some examples:

* Port meals
* Laundry service
* Delivery of courses
* Remote (the mayor or the council have the information about its implementation)
o is presented as a medallion or bracelet that is wearable continuous
o in conjunction with a central monitoring operational (24/24)
o can be coupled to a detector of activity in addition to the "beep" traditional, installed in a place of passage of the regular person

* Medical equipment

Financial aid

Several financial aid exist:

* Increase for third party of Social Security if the state of dependency has been recognized before 65
* S compensatory third person assigned by the MDPH (Departmental Office of Disability) if the patient has less than 60 years and if it is a renewal after 1 January 2006. If this is a first request this allowance is replaced by the provision of compensation aid component human There are also components of technical aids and housing development.
* Allocation personal autonomy (APA):
o attributed to the elderly (over 60) with dependent difficulties in carrying out acts of everyday life
No amount varies depending on the degree of autonomy of the elderly and resources
o the loss of autonomy is evaluated through a national grid (the grid AGGIR) which classifies the elderly in 6 groups: Group GIR1, the most dependent group GIR, the less dependent
* Housing allowances or individualized housing (APL) granted by the (Family Allowances Fund)
* Providing care at home in the CNAVTS for temporary emergency, only those whose pension fund is the main CNAVTS or CRAM (Regional Health Insurance Fund) and under certain conditions.

For material aid:

Some medical devices or equipment installed in the patient's home can be rented or purchased and paid by Social Security. For purchases and rentals important, you should seek advice and request a preliminary agreement with Social Security.

For human resources:

For the employment of anyone at home, the employer may have a tax deduction and exemption from social charges on salaries of the speaker. The APA can support the expenses of remuneration of the speaker at home if its actions are part of custom help plan prepared by the team medical and social.

Social consequences

A patient is a family that needs help. The family includes children, brothers and sisters, nieces and nephews ... Referring to the currently estimated 800 000 patients in France and by taking an average of 3 family around a patient, more than 2 400 000 people who are concerned more or less directly by Alzheimer's disease. It is a major problem for society.

In Western countries, the family has limited resources in time to give the patient the support it needs more and more continues as the evolution of the disease. Yet, in 70% of cases, the family that supports the patient and allows him to stay at home.

It has recognized the contribution of these caregivers' natural 'and professionals realize that the "Aid for caregivers" is probably one of the ways to meet this enormous public health challenge.

Demographically, the age group most affected (80 years and over) is growing. We must therefore urgently improve the system of care for people with Alzheimer's, and especially their families.

Information, training groups, respite opportunities (day care, or for specific periods) are the main ways to close for revitalization and cope with their tasks with efficiency and humanity.

Other treatments

A number of drugs tested for other diseases, were suspected at one time or another, to protect against Alzheimer's disease. This is especially some statins, some antioxidants (like vitamin E), some anti-inflammatories. These observational studies, whose original purpose was not to treat the dementia, by their essence of bias and need to be confirmed. The first results are disappointing.

Alzheimer Vaccine

The cure for Alzheimer's disease by a vaccine would be feasible, according to studies. The health of vaccinated patients showed a statistical improvement of their cognitive functions.

The idea is not new: in 1999, Dale Schenk, an American researcher, in the journal Nature a method for getting rid of the disease in mice. By immunizing against A-beta peptide transgenic mice that overexpress it comes to preventing the emergence of deposits among young animals and to limit and even reduce their extension in individuals older.

A first trial phase one in humans led to England is a success, the 80 patients treated with the support immunization and a quarter of them produce many antibodies. However, the follow-up is more mixed: while intracerebral amyloid deposits are less important, no effect on the intellectual deterioration has been proven.

NMDA antagonists

The neural receptors N-methyl-D-aspartate (NMDA) play an important role in the process of memory. It seems that when Alzheimer's disease these receptors are hyperstimulés, which would be deleterious. Memantine is an NMDA inhibitor that has been tested with contradictory results on the signs of the disease. It is for intermediate or advanced stages.

Acetylcholinesterase inhibitors

As their name suggests, they inhibit the degradation of acetylcholine, a molecule for the transmission between certain neurons in the brain through its synapses.

In 2004, several inhibitors have been tested and have shown some effectiveness, at least in mild to moderately severe: the donepezil, the rivastigmine and galantamine. In 2007 the French Commission of transparency reassessed four anticholinestérasiques and found a minor RAMS. According to the Journal prescribe their effects are modest, a few months in about 10% of patients.
The effect of these treatments is stabilizing and they do not cure the disease, or recover the existing level of performance at its onset. Their uses are exposed to many drug interactions and side effects. When a doctor decides to prescribe, they must be introduced as soon as possible without waiting for advanced stages of the disease.

Alzheimer Symptomatic treatment

They change so non-specific behavior of the patient without addressing the disease itself. Psychotropic drugs are used to reduce anxiety, aggressiveness or states of agitation of patients. Anticholinergics, neuroleptics and benzodiazepines for long half-life should be avoided because of side effects in these patients very fragile.

Alzheimer Treatment

Currently, there is no treatment curing Alzheimer's disease, or even to stop its progress, but there are few drugs that can delay the progression of the disease. They can mitigate the loss of memory, problems of language and reasoning, or simply slow down at least apparently the progression of the disease. These drugs are not permanent and are not always effective, which has been the source of controversies including their economic justification. However, even the expert bodies harshest recognize their interest.

There is another type of treatment, non-drug, namely rehabilitation: some courses allow the patient and his family live everyday with the disease, while others réhabituent the patient to live independently. The occupational therapy, aimed at raising awareness among patients, also have some effectiveness

Alzheimer Prevention

Researchers are trying to create a vaccine that would prevent dementia. This line of research remains promising.

Although there is no real way to protect themselves from disease, some people are less likely to develop the disease than others and this is usually due to their past: those who monitor Studies have long had more time to develop their memory and are therefore less likely to suffer from the disease. A diet rich in vitamins C and E would also be protective.

Today, much earlier detect Alzheimer's becomes possible. A program of artificial intelligence, born of a collaboration between two French laboratories (ESPCI-Paris-Lyon ISC) and the Japan Institute RIKEN, has learned to distinguish the warning signs of mild cognitive impairment from those moving towards this disease. The error rate is 7%.

It would be possible to divide by 2 the risk of developing Alzheimer's disease by maintaining a simple cognitive activity as read a newspaper, play chess or checkers, go to bookstores, etc.. This decrease is attributable risk that current cognitive activities of the elderly. Those practiced in the past would have no influence on the cognitive decline associated with aging.

According to research presented at the 4th International Scientific Symposium on Tea and Human Health held in Washington DC in January 2008, "green tea have a direct impact on brain function, because it contributes to the preservation these functions and to repair damaged cells. " The scientific finding that consumption of tea reduces the risk of developing dementia and other neurodegenerative diseases like Parkinson's and Alzheimer's.

Differential diagnosis

* At the initial stage of the disease, a benign forgetfulness related to age, a slight cognitive impairment or mild cognitive impairment (MCI)
* Other forms of dementia home degenerative
* Dementia called secondary (to organic)
* Anxiety disorders, depression: hence the interest of a test anxiolytic and / or antidepressants in sufficient time, the persistence of the table confirms that it is a dementia.

If this review and this test test are negative, we say that the diagnosis of Alzheimer's disease is likely; the diagnosis could not be certain that a biopsy with histological examination of the brain. There is no diagnostic certainty of life.

Alzheimer Diagnostic Certainty

Only the autopsy allows a diagnosis of certainty of Alzheimer's disease with pathological examination of the brain. In practice the diagnosis of probable Alzheimer's disease is primarily a person showing signs of gradual onset of dementia and for which other causes have been eliminated.

Alzheimer Further testing

* The brain scan or MRI can show cortical atrophy (particularly hippocampal), however (cortical atrophy or sub-cortical) is in other diseases of the elderly. Such reviews can also eliminate other causes: tumors, stroke, intra-cerebral hematoma or sub-dural, ethyl encephalopathy ... However indices are being evaluated to try to make an early diagnosis (including reducing the size of the hippocampus).
* The tomography positron emission is a recent review, allowing the analysis of some radioactive tracers injected into the body. There is a fairly sharp decrease metabolism of several parts of the brain (temporal lobe, parietal and posterior) with good sensitivity and specificity. The decrease in activity in the hippocampus would be a promising index.
* The strength in the cerebrospinal fluid of the protein t-tau protein phosphorylated tau and amyloid beta peptide of 42 amino acids allows imaging as a diagnostic aid Therefore, these assays are routinely available in some Hospitals edge.
* The dosages of vitamin B12 and vitamin B9 (folate), and a balance thyroid (TSH) are routinely made, because vitamin B12 and B9 or hypothyroidism may be causes of dementia (dementia curable).

Alzheimer Assessment Tools

All these disorders (amnesia, disturbance of executive functions, aphasia, Agnosia, apraxia) may be assessed by a psychometric testing: the MMSE (Mini Mental State Evaluation, or test Folstein), established on a scale of 30 points: a score below 24 out of 30 is suspected dementia.
This result should be interpreted according to the socioeconomic level of the patient (a high level can improve the score and therefore distort the test), and it will ensure that no confusion before its completion.

A neuropsychological evaluation can be conducted, which includes evaluation of psychometric tests, including:

* Also a MMSE (Mini Mental State Assessment Test or Folstein)
* A test called the clock (explore praxis)
* A test reminder (explores memory).

and other explorations.

Criteria of DSM-IV

The criteria of DSM-IV based on:

The installation of intellectual wearing a partial or complete:

* Memory: amnesia of recent and old
* Disorder of executive functions (ie organization and realization of a complex task, such as sheet fulfill its tax return)
* Language disorders (aphasia amnesiac) characterized by "omission of the word"
* Disorders of praxis: apraxia (ie realization of gestures complex: for example, use the washing machine)
* A Agnosia (disorders of recognition): eg road signs, faces and so on.

These disorders have an impact socio-professional.

Their evolution is a gradual and irreversible (decline ...).

These signs can not be explained by other factors, or organic (tumor, infectious, toxic) or psychological (depression, schizophrenia) and outside of acute confusion.

Alzheimer Risk Factors

• Essentially age (over 65)
• Family history of Alzheimer's, or the existence of specific mutations (presenilin, APP)
• Personal history of depression, head injury, a concept of exposure to aluminum (although these concepts are controversial)
• 4 isoform of the apolipoprotein (rarely sought)
• A diet low in polyunsaturated fatty acids omega-3 and rich in saturated fatty acids

Azheimer Diagnosis

The disease presents as a disorder of memory or behavior, evolving gradually into dementia. The cognitive impairment can be more carefully assessed by a standardized examination (form). Mood disorders are frequently associated. At a late stage is an alteration of the general state dependency with up to malnutrition, even death.

Early detection of Alzheimer's disease is a major element for better treatment and better aid for patients and their entourage.

The value of early detection of Alzheimer's disease may allow sufferers to receive treatment earlier. According to a team of French researchers, new criteria, from a combination of tests of memory, data from brain imaging and biological markers, could detect the disease at an early stage, early symptoms, " with a rate of diagnostic certainty above 90%.

The emergence of the Alzheimer's disease

In order to study the disease, mice transgenic (genetically modified) are used. In some mice, the gene encoding the Tau protein is mutated. Among others, the gene encoding the protein amyloid that is transferred. Some mice will suffer mutations in both genes.

Mice that had a mutation in the gene encoding the protein Tau show an appearance of the disease shortly pronounced. Mice that had a mutation in the gene encoding the protein amyloid behave like healthy mice. The mice with mutated genes on the two show a disease exacerbated, well defined.

This does not happen necessarily in the same way in humans, but it shows that amyloid plaques potentiate the disease. The neurofibrilles appear at first, and when the amyloid plaques appear, the disease is triggered.

The extracellular environment

In the mid extracellular protein at stake is the protein amyloid. It is a membrane protein (located on the cell membrane). This protein detaches from the membrane and enters the extracellular environment. It is then recovered and then deteriorated.

In patients with Alzheimer's disease, this degradation is not total and a fragment called amyloid-β, remains and can not be degraded. These fragments eventually aggregate and form amyloid plaques. And accumulate in the extracellular environment, these plates compress neurons. This phenomenon which leads to dysfunction, which may be followed by neuronal death.


In addition, these plaques will release a peroxide formula H2O2. The link between the two oxygen atoms are very low, it will soon "break". There will be two OH molecules, called free radicals. Free radicals do not respect the rule of bytes, they are unstable. They will seek to combine their free electron. To do so, they will push through a hydrogen atom at the membrane of the neuron (composed of carbon molecules with many hydrogen atoms). The membrane "holes" will leave penetrate other free radicals that attack the DNA of the neuron, resulting in the destruction of the cell functions of private genetic information.

The cause of accumulation also appears with normal aging, but the accumulation at the base of Alzheimer's is unknown.

The only factor is a genetic factor. This concerns another protein that act with this process of formation of amyloid plaques. She called apolipoprotein E. this depends on a protein allele may be three kinds: E2, E3 and E4.
The E2 and E3 alleles are specific to the human species. They come from a mutation of the E4 gene. The most common allele is the E3 allele (70%), followed by E4 allele (20%) then the E2 allele (10%).
The E4 allele is associated with the formation of amyloid plaques. This allele would inhibit the growth neuritique (formation of axons and dendrites). This growth allows the neuronal plasticity. This is very important for the functioning of the central nervous system. The E4 allele is therefore associated with diseases of neuronal dysfunction. The E3 allele promotes neuronal plasticity, but not as much as the E2 allele. It is for this reason that the E2 allele is associated with longevity.

The middle intracellular

In the microtubules, protein Tau placed perpendicular manner and allow the rigidity of microtubules in axonal transport.

From time to time, subject to a normal protein Tau stand out. They are replaced and degraded rapidly.
But in an affected Alzheimer's disease, Tau proteins were created from the microtubules, and fall in the intracellular environment. They are not all degraded and will therefore aggregate. That will train neurofibrilles. The neurofibrilles too important block the functioning of the neuron and do not allow the proper axonal transport. The neurofibrilles compress the neuron and cause neuronal death.

There are several explanations to the posting of Tau proteins:

* Phosphorylation: this feature allows the protein. Tau protein is phosphorylated and very little when it is very phosphorylated, it can not focus on the microtubules. These are proteins that stand out and accumulate in forming neurofibrilles. In this explanation, the cause of the increase in phosphorylation is unknown.
* Cuts proteolytiques tau proteins, which appear to intervene early and would be an event concomiant the hyperphosphorylation of these proteins.
* Genetic factors as for all the proteins, there is a gene that encodes the protein Tau. The gene may have different alleles in September. These seven alleles can be classified into two categories:
o those three reasons R
o those four grounds R.

Tau proteins derived alleles three reasons R have a fixation less important than proteins derived alleles to four reasons.

The cellular mechanisms underlying the neuronal degeneration

There are two levels of mechanisms: intra-and extracellular.
In both levels, there is an accumulation of proteins which leads to dysfunction of the cell. In the intracellular mechanisms, this accumulation is neurofibrilles. In the extracellular mechanisms, it called amyloid plaques.

Genetics of Alzheimer's disease

Genetic forms

Less than 1% patients have a disease of purely genetic origin. This form is characterized by:

* There are signs before age 60;
* An autosomal dominant (half of each generation is reached).

Two genes are involved:

* Mutation in the APP gene on chromosome 21 that encodes a precursor of the amyloid protein (five codon 717 mutations are known);
* A PSEN1 mutation on chromosome 14 (many mutations that are false sense mutations).

Genetic Susceptibility

The forms are sporadic, ie non-family, also have a genetic predisposition:

* Is the existence, discovery in 1993 of the apoE4 allele is 4 of the gene Apolipoprotein E that is significantly linked to increased risk of Alzheimer's disease. But the presence of the apoE4 is neither necessary nor sufficient to develop the disease;
* The gene Apolipoprotein E is present in three alleles: the APOE2, APOE3 and apoE4. The first is found in 51% of the population, the second occurs in 80% of the population and the third is found in 15% of the population;
* The presence of the apoE4 in the form heterozygous increases by 2 the risk of Alzheimer's disease;
* The presence of the apoE4 in the form homozygous increases by 11 the risk of Alzheimer's disease.

The apolipoprotein E intervene in neuronal repair mechanisms.

Alzheimer Anatomical Pathology

The brain of the patient with Alzheimer's disease has two types of injuries:

The senile plaques (or amyloid plaques)

This is extracellular lesions of Alzheimer's disease. These plates are the accumulation of peptide and abnormal nerve of 42 amino acids, peptide Aβ42, the most amyloidogenic amyloïde.Ce beta-peptide, normally of 40 amino acids, comes from a bad cleavage of the protein APP (amyloid protein precursor). This would participate in the massive entry of calcium into the neuron and activate microglia (inflammation), resulting in the inevitable death of the neuron by necrosis or apoptosis. These plates are mainly located in the neocortex and the hippocampus.

The neurofibrillary degeneration

These cell injury secondary to the accumulation of tau protein (protein association with microtubules that are part of the cytoskeleton) hyperphosphorylée responsible for the formation of filaments matched. When the tau protein is hyperphosphorylée it will comply with a pair of helical filaments, and then aggregate to form fibrillary neurodegeneration. The substances needed for the proper functioning of the neuron can no longer be sent to cell body and the neuron will die.

The cortical atrophy

In patients with Alzheimer's disease, the brain can lose 8 to 10% of its weight every ten years, while in healthy subjects this loss is only 2%. The cortical atrophy accompanied by an expansion of brain ventricles and cortical paths and a neuronal loss particularly affecting the cholinergic system (basal nucleus of Meynert, septum, entorhinal cortex, amygdala and hippocampus).

Alzheimer Clinical

The disease usually starts with memory disorders. Other cognitive appear gradually, leading to an array of dementia: apraxo-table-aphaso Agnos.

Alzheimer Epidemiology

There are usually a "sporadic" by far the most common in the elderly, and a "familial", starting earlier.

Alzheimer's disease for over half of all cases of dementia in the elderly. The prevalence of the disease increases sharply with age.

In Belgium, the prevalence of dementia is estimated at 5 to 10% after 65 years and almost 20% over 80 years.

In France, the study "PAQUID" (1988-2001) showed that 17.8% of people over 75 suffer from Alzheimer's disease or a related syndrome. According to a departmental assessment of 2004, about 860 000 people are affected by Alzheimer's disease in France. A figure which could reach 1.3 million in 2020 and 2.1 million in 2040. The number of new cases is about 225 000 per year.

The prevalence of the disease increases if there is a history of head injury or disease. This increase may be explained by a lysis making neuronal disease symptoms earlier.

Alzheimer History

Alois Alzheimer (1864-1915) is a psychiatrist and a German neuropathologist from the early twentieth century who studied the brains of people with dementia, through a new technique for staining with aniline and silver impregnation.

In 1906, Alois Alzheimer described for the first time the anatomical changes observed in the brain of a patient of 51 years, Auguste D. With dementia, it also presented hallucinations and abnormal orientation. In 1911, Alzheimer discovered a case similar to that of Auguste D.

It is the psychiatrist Emil Kraepelin who suggested that the disease is known as Alzheimer's, named after its discoverer.

Alzheimer's Disease

Alzheimer's disease is a neurodegenerative disease of the brain that causes progressive and irreversible loss of mental functions. It is the leading cause of dementia among older people, affecting about 24 million people worldwide.

The process responsible for the neurodegenerative disease is still poorly understood: it is due to the formation of amyloid plaques and tau protein aggregates forming the neurofibrillary degeneration. The cortical atrophy resulting in a key first time the internal temporal lobe (including the hippocampus) and the frontal cortex and associative temporo-parietal at a later stage.

The exact cause is still unknown, but it is assumed that environmental and genetic factors contribute. Mutations in at least four genes predisposing to Alzheimer's disease have been identified. They are particularly involved in familial cases early onset, which represent less than 5% of patients with Alzheimer's disease. For the so-called sporadic form of Alzheimer's disease, an increasing number of susceptibility genes (such as ApoE) have been identified.

Until the 1960s, it was assumed that the disease was rare, but later we found that in many cases, what was taken for normal aspects of senescence was in fact the disease.

The first symptom is loss of memory of recent events (amnesia) and is manifested initially by minor distractions that are gradually with the progression of the disease, while older memories are relatively preserved. Thereafter, the cognitive deficits extend to areas of language (aphasia), the organization of movements (apraxia), recognition visual (Agnosia) and executive functions (such as decision making and planning) . These symptoms reflect in particular the pathological process of degeneration reaching the frontal lobes of the brain. These changes affect the psychological qualities essential and for this reason the disease is sometimes described as a disease in which victims suffer loss of qualities that form the essence of human existence.