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Alzheimer's disease
A B C G D E F Z I K L M N O P R S T U F X C H W W E Y I
What is Alzheimer's Disease What Provokes / Causes of Alzheimer's Disease Pathogenesis (what happens?) during Alzheimer's Disease Symptoms of Alzheimer's Disease Diagnosis of Alzheimer's Disease Treatment of Alzheimer's Disease Prevention of Alzheimer's Disease Which doctors should you contact if you have Alzheimer's Disease
What is Alzheimer's Disease?
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Alzheimer's disease (also senile dementia of the Alzheimer's type) is the most common form of dementia, an incurable degenerative disease first described in 1906 by the German psychiatrist Alois Alzheimer.
As a rule, it is found in people over 65 years of age, but there is also early Alzheimer's disease - a rare form of the disease.
The global morbidity rate for 2006 was estimated at 26.6 million people, and by 2050 the number of patients may increase fourfold.
Each person has a different disease, but there are a number of common symptoms.
The first noticeable manifestations are usually mistakenly associated with old age or explained by the influence of stress.
Most often, a memory disorder is recognized in the early stages, this symptom can manifest itself, for example, by an inability to recall recently memorized information.
When contacting a doctor and Alzheimer's disease is suspected, behavior is usually analyzed to clarify the diagnosis, a series of cognitive tests are performed, if possible, magnetic resonance imaging (MRI) is performed.
With the development of the disease, symptoms such as confusion, irritability and aggressiveness, mood fluctuations, the ability to speak and understand what is said (aphasia) is impaired, there is a loss of long term memory and general self withdrawal of the patient from business as consciousness fades.
The gradual loss of body functions leads to death.
Individual prognosis is difficult due to variations in the duration of the disease, which can develop latently for a long time before symptoms become noticeable and a diagnosis is made.
The average life expectancy after diagnosis is about seven years, less than three percent of patients live more than fourteen years.
Currently, a complete understanding of the causes and course of Alzheimer's disease has not been achieved.
Studies indicate an association of the disease with the accumulation of plaques and neurofibrillary tangles in brain tissues.
Modern methods of therapy only slightly mitigate the symptoms, but so far they do not allow either to slow down or stop the development of the disease.
Many promising therapies have reached the stage of clinical trials, the number of which in 2008 was more than five hundred, but it is unclear whether their effectiveness will be proven.
There are many ways to prevent Alzheimer's disease, but their impact on the course of the disease and its severity has not been noted.
Both to prevent and to combat the disease, it is often recommended to exercise, stimulate thinking and adhere to a balanced diet.
Alzheimer's disease is one of the diseases that impose the heaviest financial burden on society in developed countries.
Epidemiology
The two main indicators used in epidemiological studies are the incidence and prevalence of the disease (morbidity).
Morbidity reflects the number of new cases per unit of person time (usually the number of new cases per thousand person years), and morbidity indicates the total number of people affected by the disease in the population at a particular time.
Cohort longitudinal studies (during which the initially healthy population is tracked for many years) indicate an incidence of 10-15 new cases per thousand person years for all types of dementia and 5-8 cases for Alzheimer's disease, which is approximately half of the total number of annual diagnoses.
Old age is the main risk factor, which is reflected in statistics: for every five years after the age of 65, the risk indicator increases approximately twice, growing from 3 cases in 65 years to 69 cases per thousand person years by 95 years.
There are also gender differences - women are more likely to develop Alzheimer's disease, especially after the age of 85.
The prevalence of the disease in the population depends on various factors, including morbidity and mortality.
Since the incidence increases with age, it is absolutely necessary to take into account the average age of the population in the study area.
In the United States, as of 2000, about 1.6 % of the population, both in general and in the 65-74 age group, had Alzheimer's disease.
In the group of 75-84 years, this indicator was already 19 %, and among citizens whose age exceeded 84 years, the prevalence of the disease was 42 %.
In less developed countries, the prevalence of the disease is lower.
According to WHO, in 2005, 0.379% of the world's population suffered from dementia, and the forecast for 2015 reaches a value of 0.441 % and an even larger percentage of the population, 0.556 %, may be affected by the disease by 2030.
The authors of other works come to similar conclusions.
Another study says that in 2006, the prevalence of the disease in the world was 0.40 % (a spread of 0.17-0.89 %, the absolute number is 26.6 million people, with a spread of 11.4-59.4 million) and predicts that the share indicator will triple, and the absolute number of patients will quadruple by 2050.
What Provokes / Causes of Alzheimer's Disease :
Microscopic image of a neurofibrillary tangle formed by hyperphosphorylated tau protein.
The explanation of the possible causes of the disease is proposed in three main competing hypotheses.
According to the oldest "cholinergic hypothesis", on which most existing therapies are based, Alzheimer's disease is caused by a reduced synthesis of the neurotransmitter acetyl choline.
Support for this hypothesis has weakened, since medications designed to correct acetylcholine deficiency have low effectiveness.
Other cholinergic effects are assumed, for example, the initiation of large scale amyloid aggregation, leading to a generalized neuroinflammatory process.
In 1991, the "amyloid hypothesis" was proposed, according to which the underlying cause of the disease is the deposition of beta amyloid (Aß).
The gene encoding the protein (APP) from which beta amyloid is formed is located on chromosome 21.
An interesting fact in support of the amyloid hypothesis is that almost all people who have lived to 40 years of age suffering from Down syndrome (an additional copy of chromosome 21 or its section), Alzheimer's like pathology is detected.
In addition, APOE4, the main genetic risk factor for Alzheimer's disease, leads to an excessive accumulation of amyloid in brain tissues even before the onset of symptoms.
Moreover, in transgenic mice whose bodies produce a mutant form of the human APP gene, fibrillar amyloid plaques are deposited in the brain and other pathological signs characteristic of Alzheimer's disease are noted.
An experimental vaccine demonstrated the ability to clear the brain of amyloid plaques in early human trials, but did not have a significant effect on dementia.
There was no strong correlation between plaque accumulation and neuronal loss.
This supports the tau hypothesis, according to which the cascade of disorders is triggered by deviations in the structure of the tau protein.
Presumably, the strands of hyperphosphorylated tau protein begin to unite with each other, eventually forming neurofibrillary tangles inside nerve cells.
This causes the disintegration of microtubules and the collapse of the transport system inside the neuron, leading first to a violation of the biochemical signal transmission between cells, and then to the death of the cells themselves.
Pathogenesis (what is happening?) during Alzheimer's Disease :
Studies of the pathogenesis and pathomorphology of Alzheimer's disease at the moment with great certainty indicate that Alzheimer's disease is most likely heterogeneous in pathogenetic terms.
Thus, one of the hypotheses of the occurrence of Alzheimer's disease is based on intracerebral amyloid deposition, which is characteristic, however, not for all cases of Alzheimer's disease.
Intracerebral deposition of pathological amyloid protein, or b amyloidprotein, in addition to Alzheimer's disease, is possible with Down syndrome, congenital cerebral hematomas with Dutch type amyloidosis and normal aging.
b amyloidprotein is an insoluble derivative of a large transmembrane glycoprotein, or amyloid precursor protein (amyloid precursor protein, APP).
The mechanism of deposition of amyloidoprotein b is currently unknown.
One of the proposed hypotheses is a point gene mutation, as a result of which a pathological b amyloidprotein is formed.
However, this hypothesis is not fully proven today.
A number of predisposing factors leading to the transition of soluble ARP to insoluble b amyloidprotein can be noted.
These are, in particular, a shift in the pH of the intercellular medium to the acidic side, insufficient mitochondrial oxidation processes, an increase in the content of free radicals.
M. D. Smyth et al. suggest that in Alzheimer's disease there is a decrease in the activity of lysosomal hydrolases, which, in turn, may be the cause of impaired resorption of amyloidprotein b.
However, in the literature devoted to the pathomorphology of Alzheimer's disease, opposite results are also given.
Fibrillar amyloid is deposited in the walls of cerebral vessels and in the parenchyma of the brain in the form of so called "senile plaques".
The deposition of amyloid leads to the death of neurons located near the senile plaques.
One hypothesis explaining this phenomenon is the activation of b amyloidotic neuronal calcium channels (with increasing levels of intracellular calcium) and the development of free radical oxidation of neuronal membranes.
A. J. Anderson et al. assume that nineronline and neuronal cell death in Alzheimer's disease the result of the expression of apoptosis growingmore (cjun) due to the impact of APP and b melodramen, which is consistent with the activation of NMD Receptorul with subsequent increased entry of Ca2+ into the cell and the development of free radical oxidation.
A direct toxic effect of amyloid on glial structures is also possible.
A. McRae et al. it has been experimentally shown that in Alzheimer's disease, microglial macrophages are activated as a result of the presumably direct toxic effect of amyloid.
This data is also confirmed by other researchers.
The result of microglia activation can be the destruction of neurons.
R. B. Banati et al. the results indicate the ability of activated microglia in Alzheimer's disease to de novo synthesize b amyloidprotein, which, accordingly, can ensure the cyclicity and progrediency of the pathological process.
Recent studies indicate the possible involvement of the complement protein in the classical pathway leading to the formation of senile plaques.
Spherical protein SP 40,40 of the human complement system in various forms is part of the amyloidoprotein b and is able to attack the complement, also containing Sprotein, through the membrane.
Activation of the classical complement cascade implements cell lysis.
In combination with reactive changes in microglia and an increase in the content of cytokines, these changes, in turn, can lead to the development of neuronal degeneration.
According to A. Afagh et al., senile plaques positive for the presence of complement are typical for Alzheimer's disease and do not occur in the absence of dementia.
Microglial reactivity and astrogliosis correlate with the presence of complement positive amyloid deposits.
Another characteristic morphological feature of Alzheimer's disease is intracellular intraneuronal plexuses, which are altered microtubules of the cytoskeleton.
The main composition of neurofibrillary plexuses is hyperphosphorylated tau protein (tauP).
Neurofibrillary plexuses are not strictly a morphological criterion for Alzheimer's disease; their presence has been described in various cerebral degenerations (frontotemporal atrophy, progressive supranuclear paralysis, etc.).
Most researchers currently deny the independent pathogenetic significance of tauP; most likely, neurofibrillary plexuses are the result of massive and generalized death of brain cells.
One of the possible components of the pathogenesis of Alzheimer's disease is the formation of pathological forms of apolipoprotein E.
Thus, according to T. Lehtimaki et al., the probability of Alzheimer's disease increases by 18 times in individuals carrying heterozygous or homozygous forms of apolipoprotein E e4.
This data is confirmed by other researchers.
The high affinity of pathological forms of apolipoprotein E to the amyloid protein and participation in the transport of tauP may contribute to the development of morphological changes characteristic of Alzheimer's disease.
Symptoms of Alzheimer's Disease :
The course of the disease is divided into four stages, with a progressive picture of cognitive and functional disorders.
Pre dementia
The first symptoms are often confused with the manifestations of aging or a reaction to stress.
The earliest cognitive difficulties are detected in some people with detailed neurocognitive testing eight years before diagnosis.
These initial symptoms can affect the performance of the most difficult everyday tasks.
The most noticeable is a memory disorder that manifests itself in difficulty when trying to recall recently learned facts and in the inability to assimilate new information.
Subtle problems of executive functions: concentration, planning, cognitive flexibility and abstract thinking, or a violation of semantic memory (memory of the meaning of words, the relationship of concepts), can also be a symptom of the early stages of Alzheimer's disease.
At this stage, apathy may be noted, which remains the most stable neuropsychiatric symptom throughout the disease.
The preclinical stage is also called "mild cognitive impairment", but there is a debate about whether to use the latter name to refer to the first stage of Alzheimer's disease or to allocate it to a separate diagnostic unit.
Early dementia
Progressive memory loss and agnosia in Alzheimer's disease sooner or later lead to confirmation of the diagnosis.
In a small number of patients, it is not memory disorders that come to the fore, but speech disorders, executive functions, perception or motor disorders (apraxia).
The disease affects different aspects of memory in different ways.
Old memories of one's own life (episodic memory), long memorized facts (semantic memory), implicit memory (unconscious "memory of the body" about a sequence of actions, for example, how to use cutlery) are less susceptible to disorder compared to new facts or memories.
Aphasia is mainly characterized by a depleted vocabulary and reduced fluency of speech, which generally weakens the ability to verbally and in writing express thoughts.
At this stage of the disease, a person is usually able to adequately operate with simple concepts in speech communication.
When drawing, writing, putting on clothes and other tasks with ispo due to the use of fine motor skills, a person may seem awkward due to certain problems with coordination and planning of movements.
As the disease develops, a person is often quite capable of performing many tasks independently, but he may need help or supervision when trying to perform manipulations that require special cognitive efforts.
Moderate dementia
The ability to act independently decreases due to the progressive deterioration of the condition.
Speech disorders become obvious, since with the loss of access to the vocabulary, a person increasingly chooses the wrong words to replace the forgotten ones (paraphrasing).
There is also a loss of reading and writing skills.
Over time, coordination is increasingly disrupted when performing complex sequences of movements, which reduces a person's ability to cope with most everyday tasks.
At this stage, memory problems increase, and the patient may not recognize close relatives.
Previously intact long term memory is also disrupted and behavioral deviations become more noticeable.
Common are such neuropsychiatric manifestations as vagrancy, evening exacerbation (English sundowning), irritability and emotional lability, manifested in crying, spontaneous aggression, or in resistance to care.
False identification syndrome and other symptoms of delirium develop in about 30 % of patients.
Urinary incontinence may develop.
In the relatives of the patient and the persons caring for him, these symptoms cause stress, which can be mitigated by moving the patient from under home supervision to an inpatient institution.
Severe dementia
In the last stage of Alzheimer's disease, the patient is completely dependent on outside help.
Language proficiency is reduced to the use of single phrases and even individual words, and as a result, speech is completely lost.
Despite the loss of verbal skills, patients are often able to understand and reciprocate emotional appeals to them.
Although at this stage there may still be manifestations of aggression, much more often the patient's condition is characterized by apathy and exhaustion, and from some point he is unable to carry out even the simplest action without someone else's help.
The patient loses muscle mass, moves with difficulty and at a certain stage is unable to leave the bed, and then eat independently.
Death usually occurs due to an external factor, such as a bedsore ulcer or pneumonia, and not due to Alzheimer's disease itself.
Diagnosis of Alzheimer's Disease :
PET brain scans for Alzheimer's disease show a decline in activity in the temporal lobes.
The clinical diagnosis of Alzheimer's disease is usually based on the patient's history (life history), the history of his relatives and clinical observations (hereditary history), while taking into account characteristic neurological and neuropsychological signs and excluding alternative diagnoses.
In order to distinguish the disease from other pathologies and varieties of dementia, complex methods of medical imaging can be used - computed tomography, magnetic resonance imaging, photon emission computed tomography or Positron emission tomography.[90]
For a more accurate assessment of the state, testing of intelligent functions, including memory, is carried out.
Medical organizations develop diagnostic criteria in order to facilitate the diagnosis of a practitioner and standardize the process of making a diagnosis.
Sometimes the diagnosis is confirmed or established postmortem by histological analysis of brain tissues.
Diagnostic criteria for Alzheimer's disease
The National Institute of Neurological and Communication Disorders and Stroke (NINDS) and the Alzheimer's Association have compiled the most commonly used set of criteria for diagnosing Alzheimer's disease.
According to the criteria, in order to make a clinical diagnosis of possible Alzheimer's disease, it is necessary to confirm the presence of cognitive impairment and suspected dementia syndrome during neuropsychological testing.
For the final confirmation of the diagnosis, a histopathological analysis of brain tissues is necessary, and during the reconciliation of lifetime diagnoses according to criteria with post mortem analysis, good statistical reliability and verifiability were noted.
Most often, disorders in Alzheimer's disease affect eight domains: memory, language skills, the ability to perceive the environment, constructive abilities, orientation in the space time of one's own personality, problem solving skills, functioning, self sufficiency.
These domains are equivalent to the NINCDS ADRDA criteria listed in DSM IV TR.
Diagnostic tools
Neuropsychological screening testing can help in the diagnosis of Alzheimer's disease, in which patients copy shapes, remember words, read, perform arithmetic operations.
PET scan: In Alzheimer's disease, the Pittsburgh compound B injected into the body accumulates in the brain, anchoring itself to the deposits of beta amyloid (left).
On the right is the brain of an elderly person without signs of Alzheimer's disease.
Neuropsychological tests, for example, MMSE, are widely used to assess cognitive impairments that should be present in the disease.
To obtain reliable results, more detailed test sets are required, especially in the early stages of the disease.
At the beginning of the disease, a neurological examination usually does not show anything unusual, except for obvious cognitive abnormalities that may resemble ordinary dementia.
In view of this, an extended neurological study is important for the differential diagnosis of Alzheimer's disease and other diseases.
A conversation with family members is also used to assess the course of the disease, since relatives can provide important information about the level of daily activity of a person and about the gradual decline in his thinking abilities.
Since the patient himself usually does not notice violations, the point of view of the people caring for him is especially important.
At the same time, in many cases, the early symptoms of dementia go unnoticed in the family and the doctor receives inaccurate information from relatives.
Additional tests enrich the picture with information about some aspects of the disease or allow you to exclude other diagnoses.
A blood test can reveal alternative causes of dementia, which sometimes even respond to therapy that reverses the symptoms.
Psychological tests are also used to detect depression, which can both accompany Alzheimer's disease and cause cognitive decline.
SPECT and PET imaging equipment, if available, can be used to confirm the diagnosis together with other assessment methods, including mental status analysis.
In people who already suffer from dementia, SPECT, according to some data, allows you to more effectively differentiate Alzheimer's disease from other causes, compared with standard testing and anamnesis review.
The opportunity to observe the deposits of amyloid beta in the brain of living people appeared thanks to the creation of the University of Pittsburgh composition B (PiB), which binds to amyloid deposits when injected into the body.
The short lived radioactive isotope carbon 11 in the compound allows determining the distribution of this substance in the body and obtaining a picture of amyloid deposits in the patient's brain using a PET scanner.
It is also shown that the content of beta amyloid or tau protein in the cerebrospinal fluid can be an objective marker of the disease.
These two new methods have led to proposals for the development of new diagnostic criteria.
Treatment of Alzheimer's Disease :
There is no cure for Alzheimer's disease; the available therapies can slightly affect the symptoms, but are essentially palliative measures.
Pharmacological, psychosocial and patient care measures can be distinguished from the whole range of measures.
Pharmacotherapy
Regulatory agencies such as the FDA and EMEA have currently approved four drugs for the treatment of cognitive impairment in Alzheimer's disease - three cholinesterase inhibitors and memantine, an NMDA antagonist.
At the same time, there are no such drugs, among the actions of which it would be indicated to slow down or stop the development of Alzheimer's disease.
A well known sign of Alzheimer's disease is a decrease in the activity of cholinergic neurons.
Cholinesterase inhibitors reduce the rate of destruction of acetylcholine( ACh), increasing its concentration in the brain and compensating for the loss of ACh caused by the loss of cholinergic neurons.
As of 2008, doctors used such ACh inhibitors as donepezil, galantamine, and rivastigmine (in the form of tablets and patches) There is evidence of the effectiveness of these drugs at the initial and moderate stages, as well as some grounds for their use at a late stage.
Only donepezil is approved for use in the onset of severe dementia.
The use of these drugs in mild cognitive impairment did not slow down the onset of Alzheimer's disease.
Among the side effects of drugs, the most common are nausea and vomiting associated with an excess of cholinergic activity, they occur in 10-10% of patients and can be weakly or moderately expressed.
Muscle spasms, bradycardia, decreased appetite, weight loss, increased acidity of gastric juice are less common.
Excitatory neurotransmitter glutamate plays an important role in the nervous system, but its excess leads to excessive activation of glutamate receptors and can cause cell death.
This process, called excitotoxicity, is noted not only in Alzheimer's disease, but also in other conditions, for example, in Parkinson's disease and multiple sclerosis.
A drug called Memantine, originally used in the treatment of influenza, inhibits the activation of glutamate NMDA receptors.
Memantine has been shown to be moderately effective in moderate to severe Alzheimer's disease, but it is not known how it acts at an early stage.
Rarely there are mild side effects, among them - hallucinations, confusion, dizziness, headache and fatigue.
In combination with donepezil, memantine demonstrates "statistically significant, but clinically barely noticeable effectiveness" in acting on cognitive indicators.
In patients whose behavior is a problem, antipsychotics can moderately reduce aggression and affect psychosis.
At the same time, these drugs cause serious side effects, in particular, cerebrovascular complications, motor disorders and a decrease in cognitive abilities, which excludes their daily use.[151][152]
With prolonged administration of antipsychotics in Alzheimer's disease, there is an increased mortality rate.
Psychosocial intervention
"Sensory integrative therapy": a special sensory room (English snoezelen) is used for emotionally oriented assistance to people suffering from dementia.
Psychosocial intervention complements pharmacological intervention and can be divided into the following approaches:
- behavioral;
- emotional;
- cognitive;
- stimulant oriented.
The effectiveness of the intervention is not yet covered in the scientific literature, besides, the approach itself does not apply to Alzheimer's disease, but to dementia in general.
Behavioral intervention is aimed at identifying the prerequisites and consequences of problematic behavior and working to correct them.
When using this approach, there was no improvement in the overall level of functioning, but it is possible to mitigate some individual problems, such as urinary incontinence.
There is not enough qualitative data on the impact of methods of this direction on other behavioral deviations, such as wandering.
Interventions affecting the emotional sphere include reminiscence therapy (RT), validation therapy, supportive psychotherapy, sensory integration ("snuzelen"), and "simulated presence therapy" (SPT).
Supportive psychotherapy has hardly been studied by scientific methods, but some clinical workers believe that it provides benefits when trying to help patients with mild illness adapt to the disease.
In memory therapy (RT), patients discuss their experiences face to face with a therapist or in a group, often using photographs, household items, old music and archival audio recordings, and other familiar objects from the past.
Although the number of qualitative studies of the effectiveness of RT is small, there may be a positive impact of this method on the patient's thinking and attitude.
The simulation of presence, based on attachment theories, involves playing audio recordings with the voices of close relatives.
According to preliminary data, the level of anxiety decreases in patients undergoing SPT, their behavior becomes calmer.
Validation therapy is based on the recognition of the reality and personal truth of another person's experiences, and during sensory integration sessions, the patient performs exercises designed to stimulate the senses.
There is not much data to support these two methods.
Reality orientation, cognitive retraining, and other cognitively oriented therapies are used to reduce cognitive deficits.
Orientation in reality consists in presenting information about the time, location and personality of the patient in order to facilitate their awareness of the situation and their own place in it.
In turn, cognitive retraining is carried out to improve the impaired abilities of the patient, who is given tasks that require mental stress.
There was some improvement in cognitive capabilities when using as a pe both the first and the second method, however, in some studies this effect disappeared over time and negative manifestations were noted, for example, patient disappointment.
Stimulating methods of therapy include art therapy, music therapy, as well as types of therapy in which patients communicate with animals, engage in physical exercises and any other restorative activity.
According to studies, stimulation has a moderate effect on behavior and mood, and even less on the level of functioning.
Anyway, such therapy is carried out mainly to improve the daily life of patients.
Prevention Of Alzheimer's Disease :
Intellectual activity, including a passion for playing chess, and regular communication correlate with a reduced risk of developing Alzheimer's disease, according to epidemiological studies, but a causal relationship has not yet been proven.
International studies designed to assess how much a particular measure can slow down or prevent the onset of the disease often give contradictory results.
To date, there is no solid evidence of the preventive action of any of the factors considered.
At the same time, epidemiological studies suggest that some correctable factors - diet, risk of cardiovascular diseases, medication intake, mental activity, and others - are associated with the likelihood of developing the disease.
However, real evidence of their ability to prevent the disease can be obtained only in the course of additional research, which will include clinical studies.
The ingredients of the Mediterranean diet, including fruits and vegetables, bread, wheat and other cereals, olive oil, fish and red wine, may be able to individually or together reduce the risk and mitigate the course of Alzheimer's disease.
Taking some vitamins, including B12, B3, C and folic acid, has been associated with a reduced risk of developing the disease in some studies, but other studies indicate that there is no significant effect on the onset and course of the disease and the likelihood of side effects.
Curcumin, contained in a common spice, in a study on mice showed some ability to prevent certain pathological changes in the brain.
Risk factors for cardiovascular diseases, such as high cholesterol and hypertension, diabetes, smoking, are associated with an increased risk and a more severe course of Alzheimer's disease, but cholesterol lowering drugs (statins) have not shown effectiveness in preventing it or improving the condition of patients.
Long term use of nonsteroidal anti inflammatory drugs is associated with a reduced probability of developing the disease in some people.
Other medications, such as hormone replacement therapy in women, are no longer considered effective in preventing dementia.
A systematic review of ginkgo biloba conducted in 2007 indicates the inconsistent and inconclusive nature of the presented evidence of the drug's effect on cognitive impairment, and another study indicates that there is no effect on morbidity.
Intellectual activities, such as reading, board games, solving crosswords, playing musical instruments, regular communication, may be able to slow down the onset of the disease or mitigate its development.
Bilingual proficiency is associated with a later onset of Alzheimer's disease.
Some studies suggest an increased risk of developing Alzheimer's disease in those people whose work is associated with exposure to magnetic fields, ingestion of metals, especially aluminum, or the use of solvents.
Some of these publications have been criticized for the poor quality of the work, besides, other studies have not found a link between environmental factors and the development of Alzheimer's disease.
Which doctors should you contact if you have Alzheimer's disease :
Psychiatrist
Neurologist
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From you ?
It is necessary to take a very careful approach to the state of your health in general.
People do not pay enough attention to the symptoms of diseases and do not realize that these diseases can be life threatening.
There are many diseases that do not manifest themselves in our body at first, but in the end it turns out that, unfortunately,it is too late to treat them.
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Other diseases from the group Mental disorders and behavioral disorders:
Agoraphobia
Agoraphobia (fear of empty spaces)
Anancastic (obsessive compulsive) personality disorder
Anorexia nervosa
Asthenic disorder (asthenia)
Affective disorder
Affective mood disorders
Insomnia of an inorganic nature
Bipolar affective disorder
Bipolar affective disorder
Delusional disorder
Delusional disorder
Bulimia nervosa
Vaginismus of an inorganic nature
Voyeurism
Generalized anxiety disorder
Hyperkinetic disorders
Hypersomnia of an inorganic nature
Hypomania
Motor and volitional disorders
Delirium
Delirium not caused by alcohol or other psychoactive substances
Dementia in Alzheimer's disease
Dementia in Huntington's disease
Dementia in Creutzfeldt Jakob disease
Dementia in Parkinson's disease
Dementia in Pick's disease
Dementia in diseases caused by the human immunodeficiency virus (HIV)
Recurrent depressive disorder
Depressive episode
Depressive episode
Children's autism
Disocial personality disorder
Dyspareonia of inorganic nature
Dissociative amnesia
Dissociative amnesia
Dissociative anesthesia
Dissociative fugue
Dissociative fugue
Dissociative disorder
Dissociative (conversion) disorders
Dissociative (conversion) disorders
Dissociative motor disorders
Dissociative motor disorders
Dissociative seizures
Dissociative seizures
Dissociative stupor
Dissociative stupor
Dysthymia (depressive mood)
Dysthymia (mood decline)
Other organic personality disorders
Dependent personality disorder
Stuttering
Induced delusional disorder
Hypochondriac disorder
Hysterical personality disorder
Catatonic syndrome
Catatonic disorder of an organic nature
Nightmares
A mild depressive episode
Mild cognitive impairment
Manic episode
Mania without psychotic symptoms
Mania with psychotic symptoms
Violation of activity and attention
Violation of psychological development
Neurasthenia
Undifferentiated somatoform disorder
Inorganic encopresis
Inorganic enuresis
Obsessive compulsive disorder
Obsessive compulsive disorder
Orgasmic dysfunction
Organic (affective) mood disorders
Organic amnesic syndrome
Organic hallucinosis
Organic delusional (schizophrenic) disorder
Organic dissociative disorder
Organic personality disorder
Organic emotionally labile (asthenic) disorder
Acute reaction to stress
Acute reaction to stress
Acute polymorphic psychotic disorder
Acute polymorphic psychotic disorder with symptoms of schizophrenia
Acute schizophrenic like psychotic disorder
Acute and transient psychotic disorders
No genital reaction
Lack or loss of sexual desire
Panic disorder
Panic disorder
Paranoid personality disorder
Pathological tendency to gambling (ludomania)
Pathological arson (pyromania)
Pathological theft (kleptomania)
Pedophilia
Increased sexual desire
Eating inedible (peak) in infancy and childhood
Post concussion syndrome
PTSD
Post traumatic stress disorder
Postencephalitic syndrome
Premature ejaculation
Acquired aphasia with epilepsy (Landau Kleffner syndrome)
Mental and behavioral disorders due to alcohol consumption
Mental and behavioral disorders due to the use of hallucinogens
Mental and behavioral disorders due to the use of cannabioids
Mental and behavioral disorders due to cocaine use
Mental and behavioral disorders due to caffeine use
Mental and behavioral disorders due to the use of volatile solvents
Mental and behavioral disorders due to opioid use
Mental and behavioral disorders due to the use of psychoactive substances
Mental and behavioral disorders due to the use of sedatives and hypnotics
Mental and behavioral disorders due to tobacco use
Mental and behavioral disorders associated with the postpartum period
Intellectual disorders
Behavioral disorders
Disorders of sexual identification in children
Disorders of habits and drives
Disorders of sexual preference
Sleep disorders of an inorganic nature
Disorders of emotions and affect
Perception and imagination disorder
Personality disorder
Multiple personality disorder
Thinking disorder
Memory and attention disorder
Eating disorder in infancy and childhood
Puberty disorder
Disorder of adaptive reactions
Receptive speech disorder
Sexual connection disorder
Disorder of consciousness
Expressive speech disorder
Recurrent depressive disorder
Speech excitedly
Sado masochism
Sexual aversion and lack of sexual satisfaction
Stendhal Syndrome
Asperger's syndrome (autistic psychopathy, schizoid disorder of childhood)
Geller syndrome (symbiotic psychosis, childhood dementia, Geller - Zappert disease)
De la Tourette Syndrome
Lennox - Gastaut syndrome
Otahara Syndrome
Rasmussen's progressive encephalopathy syndrome
Rett Syndrome
West's Syndrome
Sleepwalking (somnambulism)
Somatized disorder
Somatoform dysfunction of the autonomic nervous system
Somatoform disorders
Somatoform disorders
Somatoform disorders
Vascular dementia
Vascular dementia
Social phobias
Specific (isolated) phobias
Specific personality disorders
Specific speech development disorders
Specific disorders of the development of school skills
Specific speech articulation disorder
Specific disorder of the development of motor functions
Tic disorders
Transient tic disorder
Trance and obsession
Double role transvestism
Transsexualism
Trances and states of mastery
Anxiety phobic disorders
Anxiety (evasive) personality disorder
Anxiety disorder
An anxiety disorder of an organic nature
Trichotillomania (tendency to pull out hair)
Severe depressive episode without psychotic symptoms
Severe depressive episode with psychotic symptoms
Horrors during sleep (night terrors)
Moderate depressive episode
Mental retardation
Febrile convulsions
Fetishism
Fetishistic transvestism
Specific (isolated)phobias
Phobic
