Senile dementia has become the third leading health problem in overdeveloped countries, behind cardiovascular accidents and cancer. The growing public, biomedical and political interest in dementia stems from the marked increase in its prevalence in Western societies. The longevity of those over 65 years of age has increased dramatically in the past decades. Life expectancy in the developed world has reached 82 years, increasing the risk of dementia. Severe dementia is increasing by 25%.
Characteristics and symptomatology of dementia
It is now accepted that dementia is a symptomatic complex that can be caused by more than 70 different pathological processes. Symptoms of dementia include:
– loss of recent memory
– loss of language functions
– inability to think abstractly
– inability for self-care
– personality disorder
– emotional instability
– loss of sense of time and space
These characteristics differentiate dementia from mental retardation in that they are mental faculties that are lost once acquired and exercised over a long period of time, while in mental retardation they are never fully possessed. Dementia also differs from delirium in that the latter presents with a drop in attention and temporary confusion, accompanied by transient loss of certain cognitive functions, depending on the agent responsible for the delirium.
The first indication of senile mental deficiency is found in the Law of Solon written in Greece around 400 B.C. Subsequently, in the first century of our era, A. Cornelius Celsius introduced the terms dementia and delirium in his work De Medicina in Rome. Likewise, Galen coined the term morosis as a synonym for dementia. It was in 1906 when Alosius Alzheimer, a German neurologist, presented the case of a 51-year-old patient with dementia, and discovered changes in the neurofibrillae or neurofibrillary tangles. The patient presented disorientation, jealousy, memory loss, perceptual deficits, aphasia, apraxia, agnosia, paraphasia, persecutory mania, abnormal behaviors and rapid progression of the disease. The Germanic school of Krepelin and later Fisher discovered the so-called senile plaques with amyloid content in the brain pathology.
Types of dementias
Scientific research on the pathology of Alzheimer’s disease has led to deepen and clarify the classification of dementias into two major groups:
– Taupathies: They are related to the alteration of the Tau Protein. The following dementias are included in this group: Alzheimer’s disease, frontotemporal dementia, cortico-basal dementia, progressive supranuclear palsy, Pick’s disease, Creutzfeldt-Jacob disease, Gersman’s disease, Strausler’s disease and primary progressive aphasia.
– Synucleopathies: It is a multisystem atrophy, nicro-striatal degeneration and olivopontocerebellar atrophy. It is a dementia associated with Parkinson’s disease and dementia with Lewy bodies. Parkinson’s disease carries a six times higher risk of developing dementia than in the healthy population.
Etiology or causes of Alzheimer’s disease
Despite the efforts made in the last 20 years to identify the factor or factors involved in the genesis of Alzheimer’s disease, its cause still remains an enigma. Etiopathogenic theories of Alzheimer’s disease have been considered for years:
1) Cholinergic deficit
2) Genetic failure
3) Accumulation of abnormal proteins
4) Infectious agent
5) Environmental toxin
6) Deficient cerebral flow
7) Neuroimmune disorder
8) Secondary traumatic and psychosocial factor.
From the genetic point of view, some families show a hereditary pattern, caused by genetic mutations in chromosomes 1, 14 and 21. This is the case of some patients with early onset, before the age of 65 years, which affects less than 10% of Alzheimer’s patients. Although no specific gene has been identified in late-onset Alzheimer’s disease, genetic factors play a role in the development of the disease. Some examples are the ApoE gene in its three forms E2, E3, E4, on chromosome 19, where the E4 form is more likely to develop the disease.
On the other hand, an abnormal protein called beta amyloid protein is deposited in the neurons of Alzheimer’s patients, which progressively destroys the neurons. There is also a deficit in the brain of the neurotransmitter acetylcholine.
Vitamin D deficiency and a history of cranial trauma are also hypotheses about the cause of this disease, as well as excessive aluminum deposition.
Abnormal deposition of so-called TAU proteins and brain synucleoproteins are the subject of current research in Alzheimer’s disease.
Symptoms of Alzheimer’s disease
Symptomatology of this disease includes:
– Cognitive and motor symptoms: amnesia, language aphasia, apraxia (dressing), agnosia, failure to recognize faces or the disease itself, learning disorder, disorientation, seizures, muscle contractures and motor incoordination.
– Functional symptoms: difficulty walking, difficulty eating, difficulty maintaining the home, difficulty dressing and grooming, difficulty with financial management.
– Behavioral symptoms: catastrophic reactions, fits of rage, manic-depressive episodes, violence, apathy, wandering, sleep disorders, obscene language, hallucinations, delusions, paranoia, judgment disorder, sexual disorders, social maladjustment, akathisia or personality disorders.
– Associated symptoms: delirium, gustatory, auditory, visual or olfactory hallucinations.
Diagnosis and treatment of Alzheimer’s disease
Tests in the diagnostic process are an important tool. Among them are: Pet Amyloid scanner, Electroencephalogram, Neuropsychological Study, General Analytical, Thyroid tests, Vitamin B12, Folic Acid, Cerebrospinal Fluid (CSF) Analysis: Amyloid Deta and Tau Protein.
Current treatments are:
– Inhibition of the enzyme that metabolizes the neurotransmitter acetyl choline. It is a target in current treatment, orally or in the form of transdermal patches with drugs such as rivastigmine, donepecilo or galantamine.
– Cognitive stimulation therapy. Psychotherapy and psychosocial support are essential in the management and treatment of Alzheimer’s disease. Admission to 24-hour nursing homes or day centers are necessary in some cases.
– Current research is trying to act against the process that produces the abnormal beta amyloid protein in the brain, since this protein deposited in neurons destroys them. In this regard, the experimental EB1D vaccine, a new immunogen that generates antibodies against the neuritic plaques where the beta-amyloid protein accumulates, has been tested.
– Atypical neuroleptics are also administered for delusions, hallucinations and behavioral disorders. Also serotonin reuptake inhibitors and other non-tricyclic antidepressants.
– Psychological care for the caregivers of these patients.
In general, Neurology experts have high expectations regarding the treatment of Alzheimer’s disease, whose investment in research is already bearing fruit.