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Alzheimer dementia: A problem of individuals, families, medicine and society
Author(s) -
Smiljana Kostić
Publication year - 2015
Publication title -
vojnosanitetski pregled
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.123
H-Index - 19
eISSN - 2406-0720
pISSN - 0042-8450
DOI - 10.2298/vsp1509763k
Subject(s) - dementia , medicine , alzheimer's disease , psychiatry , gerontology , psychology , disease , pathology
Since ancient times the term dementia, derived from the Latin word demeans ("no mind"), has marked a specific, acquired state of impaired intellectual and mental abilities of an adult which interfere with his her social and working abilities, making him her dependent on others. At the beginning of the 2nd century Roman poet Junius Juvenal described how the weakness of the mind is worse than any physical illness, "Sed omni membrorum damno maior dementia, quae nec nomina servorum nec vultum agnoscit amici cum quo praeterita cenavit nocte, nec illos quos genuit, quos eduxit". ("But worse than any loss in body is the failing mind which forgets the names of slaves, and cannot recognize the face of the old friend who dined with him last night, nor those of the children whom he has begotten and brought up"). According to the assessment of the group of experts commissioned by the Alzheimer Disease International in 2005 about 24 million people suffered from dementia at that time, with 4.6 million new cases arising every year . The lifespan of the world's population has extended and there is a trend of increase of the elderly population. It is predicted that in 20 years the number of people affected by dementia will be nearly doubled. A frightening prediction says that by the year 2050 115 million people will be suffering from this disease and that 1 out of 85 persons will be demented. Alzheimer dementia (AD) is the most common and accounts for about 70% of all dementias. The prevalence rates increase with age and double every 5 years after age 65. Based on its age of onset, AD is classified into early onset AD, before the age of 65, accounting for 1–5% of all cases, and late-onset AD, after the age of 65, which occurs in 95% of patients. Although there are no significant differences in the clinical symptoms of the two types of the disease, it is considered that the early onset AD is connected with faster progression and a different inheritance patterns. Mutations in three genes (APP, PSEN1, PSEN2) that participate in the encoding of proteins involved in the pathophysiological processes of the synthesis of the amyloid precursor protein and amyloid-beta (Aβ) are inherited autosomal dominant with high penetrance. In late-onset sporadic form there is an increased tendency towards manifestations of the disease in relatives of the patients, and the risk is doubled if the disease exists in the first instance relatives. AD is result of a progressive neurodegenerative process whose pathological characteristics represent diffuse extracellular senile plaques made up of Aβ and intracellular neurofibrillary tangles consisting of tau protein aggregates, associated with reactive microgliosis, dystrophic neurites and neuronal and synaptic loss. In its clinical course this multifactorial neurodegenerative disease progresses from the prodromal phase to the late stages and histopathological substrate often cannot fully explain the clinical features of the disease. Today we know that the pathological process begins decades before the first manifestation of the clinical symptoms and it is still assumed that the disorder of Aβ protein metabolism, the amyloid cascade, in the central nervous system is the initial and significant factor causing the disease. Hence, the main therapeutic strategies aim at modifying the abnormal production, accumulation and depositing of Aβ. Application of drugs that could potentially change the course of the disease would find its place in the earliest stages, asymptomaticmolecular, prodromal and early onset AD. Until recently, the diagnosis of the disease, according to the valid criteria of Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer Disease and Related Disorders Association (NINCDSADRDA) from 1984, relied mainly on clinical characteristics of the disease reaching the reliability level of probable, but definite diagnosis requested an autopsy, histopathologic confirmation. In the light of new knowledge, with a reliable and early recognition of the disease being the aim, diagnostic criteria

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