Alzheimer's disease (AD) has become a growing problem in the medical, psychiatric, neurological, epidemiological, social and economic order, particularly in countries with a high life expectancy
Alzheimer's dementia can be classified according to the age of onset in presenile or early onset, which appears before age 65 and senile or late onset, ie onset after age 65. It according to the presence or absence of a family history of the disease is classified into familial AD and sporadic AD, respectively. However, these classifications are not mutually exclusive.
The development achieved by genetic has demonstrated the involvement of several chromosomes in the development of the disease. Chromosomes 1, 14 and 21 are associated with familial forms of start precoz. While late onset forms appear linked to chromosomes 12 and 19
In this paper we delved into the study of chromosome 21 and the amyloid beta protein, because there are many findings that relate to deposit excess amounts of this protein among the leading causes of disease. Furthermore, aspects of chromosome 17 and treated Tau protein, because the latter is the main constituent of neurofibrillary tangles, whose number is directly related to the severity of dementia. However it is important to note that these are not the only issues involved in the pathogenesis of the disease.
The first incident involving chromosome 21 AD broke that individuals with Down syndrome (trisomy 21) invariably developed clinicopathological features of the disease, if they lived above the 30 years. Subsequent studies of senile plaques, first observable event in AD pathology, showed that its main constituent was the beta amyloid (SSA).
Amyloid plaques and neurofibrillary tangles are neuropathological hallmark lesions of Alzheimer disease (AD) The most common form of neurodegenerative disorder. Neurofibrillary tangles are intracellular hyperphosphorylated Tau inclusions FORMED of Plaques are extracellular inclusions mainly formed of a small peptide called amyloid-β (Aß). Clinically, AD is Characterized by profound memory loss and cognitive dysfunction. Growing evidence is converging on soluble Aß as a mediator of early cognitive decline in AD. , Although the Molecular Mechanisms underlying Aß-induced cognitive decline remain elusive, soluble Aß oligomers shown to alter Have Been signal transduction pathways are key for That learning and memory, suggesting That Alterations in May Such pathways underlie the onset of cognitive decline in AD
Alzheimer's dementia can be classified according to the age of onset in presenile or early onset, which appears before age 65 and senile or late onset, ie onset after age 65. It according to the presence or absence of a family history of the disease is classified into familial AD and sporadic AD, respectively. However, these classifications are not mutually exclusive.
The development achieved by genetic has demonstrated the involvement of several chromosomes in the development of the disease. Chromosomes 1, 14 and 21 are associated with familial forms of start precoz. While late onset forms appear linked to chromosomes 12 and 19
In this paper we delved into the study of chromosome 21 and the amyloid beta protein, because there are many findings that relate to deposit excess amounts of this protein among the leading causes of disease. Furthermore, aspects of chromosome 17 and treated Tau protein, because the latter is the main constituent of neurofibrillary tangles, whose number is directly related to the severity of dementia. However it is important to note that these are not the only issues involved in the pathogenesis of the disease.
The first incident involving chromosome 21 AD broke that individuals with Down syndrome (trisomy 21) invariably developed clinicopathological features of the disease, if they lived above the 30 years. Subsequent studies of senile plaques, first observable event in AD pathology, showed that its main constituent was the beta amyloid (SSA).
Amyloid plaques and neurofibrillary tangles are neuropathological hallmark lesions of Alzheimer disease (AD) The most common form of neurodegenerative disorder. Neurofibrillary tangles are intracellular hyperphosphorylated Tau inclusions FORMED of Plaques are extracellular inclusions mainly formed of a small peptide called amyloid-β (Aß). Clinically, AD is Characterized by profound memory loss and cognitive dysfunction. Growing evidence is converging on soluble Aß as a mediator of early cognitive decline in AD. , Although the Molecular Mechanisms underlying Aß-induced cognitive decline remain elusive, soluble Aß oligomers shown to alter Have Been signal transduction pathways are key for That learning and memory, suggesting That Alterations in May Such pathways underlie the onset of cognitive decline in AD
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