Amyloid precursor protein

memory loss, changes in personality and confusion (among a plethora of other symptoms). Physiologically, the disease is characterized by the accumulation of insoluble amyloid beta plaques, derived from the amyloid precursor protein (APP). Another characteristic marker for Alzheimer’s dementia is the Hyper-phosphorylation of the Tau protein which then aggregates to form insoluble neurofibrillary tangles (NFTs), that inhibit a cell’s ability to regulate the stabilization of the microtubule component tubulin

Alzheimer’s Disease: Genetic Analysis Introduction Alzheimer’s disease (AD) is a profoundly common form of degenerative dementia that is caused by neurofibrillary tangles and amyloid plaques accumulating in the brain (Sennvik et.al., 2000). The study of the human genome has elucidated gene variants; single nucleotide polymorphisms (SNPs) and mutations which affect the age of onset and the likelihood of developing AD. Understanding the causes of familial AD, the genetic risk factors for AD and the

In damaged regions of the brain, the dysfunction and death of neurons is associated with cytoskeletal abnormalities and results in a reduction in the level of synaptic proteins in the regions of the brain within which these neurons terminate. The distribution and the spread of these abnormalities follow characteristic patterns that are area-specific and even cell-specific. Normal neurons contain neurofilaments, but no neurofibrillary

on Aging). According to recent research, it is believed that Alzheimer’s is caused due to a build up of a protein, called beta-amyloid. This protein peptide is toxic and insoluble, and forms more predominantly in particular regions of the brain, compared to the plaque buildup in a healthy aging person’s brain. Beta-amyloid proteins form from a protein known as amyloid precursor protein (APP), which

Unfortunately, I have seen first-hand the devastation Alzheimer’s disease causes in someone’s life. My best friend’s aunt, and my Great Aunt were both diagnosed with Alzheimer’s when I was in grade school. I didn’t know anything about this disease, I only saw the progression and the clinical manifestations of the disease. The second aspect of Alzheimer’s that I didn’t understand was how doctors weren’t able to cure this disease. Our textbook, McCance and Huether state, “Some diseases, such as tuberculosis

of plaque and dysfunctional proteins in the brain interfering with neuronal function. Alzheimer’s disease (AD) is an age-related neurodegenerative disease that accounts for more than 60 % of all dementia cases. The disease is characterized by cognitive deficits and memory loss through a process that lead to the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs). This plaque is composed of abnormally hyperphosphorylated tau protein in the brain. Amyloid beta (Aβ or Abeta) is a peptide

inherited genetic factors. The most known and possible factors of FAD type are attributed to be autosomal dominant mutations within three important genes, which are genes encoding for amyloid precursor protein (APP) and presenilins 1 and 2 (PS1 and PS2), and both of which could result to increase the production of beta-amyloids especially Aβ40 (Chadwick et al.,

Japan had discovered how to detect Alzheimer disease much sooner than before through blood test. Through the measurement of amyloid-β proteins and its precursors in the blood, doctors can detect Alzheimer disease sooner. One of the earliest hallmark of Alzheimer disease is the accumulation of amyloid-β proteins. Prior to this discovery, in order to measure the proteins, the procedure

relationship between cognitive decline and the number of plaques in the brain. In the 1970’s AD was documented as the most common type of dementia (Bright Focus Foundation, 2015). In 1984 another ground breaking discovery was made. In 1984 the Beta-Amyloid was discovered by George Glenner and Cai 'ne Wong (Alzheimer’s Association, 2015). In the 1990 's a few more discoveries were made, such as complex nerve cells, and genetics coincident, and AD susceptibility. However, the last decade has been crucial

pathogenesis of AD: Amyloid cascade hypothesis The β-amyloid plaques are an extracellular deposition of amyloid beta protein[21]. This protein is derived from cleavage of the amyloid precursor protein (APP) by the β - and γ- secretase enzymes [22] . The accumulated amyloid bet npeptides can aggregatr into oligomer (24) And form plaques (16) The Aβ deposition and diffused plaque formation lead to local microglial activation, cytokine release, reactive astrocytosis and a multi-protein inflammatory response