Amyloid

as well as extracellular A-beta amyloid. These lesions are surrounded by microglial and astrocytes. The brain regions affected by Alzheimer’s disease also contain neuritic or senile plaques in which extracellular deposits of amyloid are surrounded by dystrophic axons as well as the process of astrocytes and microglia. The principle constituent of amyloid is a 4kDa peptide called A-beta amyloid. A-beta amyloid is cleaved from a larger precursor protein called amyloid precursor protein. Similar abnormalities

reduce Aβ accumulation may be their most important neuroprotective action against cognition decline. As mentioned previously, Aβ formation from APP mediated by two pathways either amyloid genic or non-amyloid genic routes. If the production of low levels of soluble APP alpha by non-amyloid genic route and factors influence amyloid genic processing of APP or a reduction in the Aβ clearance pathways can lead to accumulation of Aβ, which in turn promotes assembly of the Aβ peptides into toxic oligomers and

Relationship between Alzheimer Disease and Down syndrome Down Syndrome (DS) is a genetic and developmental disorder that arises due to a certain biological defect during the fusion of gametes to produce a new organism. The occurrence of his biological defects leads to an extra partial or full copy of chromosome 21 in every cell in the individual’s body. In other words, there are more copies of chromosome 21 in every cells in that person’s body instead of the normal pairs. According to the article

Current & Future AD Drug Development & Associated Obstacles With 46.8 million people currently living with AD and the number of people to be diagnosed in the future set to rise, a study conducted by (Cummings, Morstorf & Zhong 2014) analysed the clinical trials associated with Alzheimer’s drug development throughout 2002 to 2012 in USA listed on clinicaltrials.gov. The united states undertakes the largest number of clinical trials compared to anywhere else in the world; in total 413 trials had

Prions are infectious protein agents that cause aggregation of the peptide PrPC and form large amyloid fibrils. These fibrils resist proteoysis and can have a detrimental effect of the functionality of cells and ultimately cause their death. (3). Misfolded PrPC will form stable aggregates denoted as PrPSc. PrPC is a soluble protein that is present in all organism whose function is still not totally clear (3). When PrPc converts to PrPSc there is an increase in the number of β sheets in the protein

structural support collapses. Plaques, or clumps of fibres, form outside the neurons in the adjacent brain tissue. Scientists found that a type of protein, called amyloid precursor protein, forms toxic plaques when it is cut in two places. Researchers have isolated the enzyme beta-secretase, which is believed to make one of the cuts in the amyloid precursor protein. Researchers also identified another enzyme, called gamma secretase that makes the second cut

criteria addressed the disease and described only later stages, when symptoms of dementia were already evident. It was assumed that people free of dementia symptoms were disease-free. Diagnosis was confirmed only at autopsy, showing abnormal amounts of amyloid proteins forming plaques and tau proteins forming tangles found in the brain. The updated guidelines cover the full continuum of the disease as it gradually progresses over many years. They describe the earliest preclinical stages of the disease

presence of plaques and neurofibrillary tangles. (18 -20) There are two main hypotheses explaining the 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

1.4. Diagnosis The only sure way to confirm diagnosis of AD is the autopsy of brain tissue and finding the characteristic gross pathological findings of the disease. But this procedure takes place after the death of the patient. However, diagnosis can be accomplished with high accuracy even when the patient is still alive with a variety of methods (Medline plus, 2010):  Careful and detailed clinical examination by experienced and qualified neurologist.  Neuropsychological testing, which is necessary

by detecting beta-amyloid in the brain. In cardiology, it measures cardiac perfusion and assesses pathogenesis of intractable cardiac pathology (Batsuri, 2015). Sevigny et al., (2016), studied PET as a diagnostic tool to identify the AD patient with positive amyloid. The authors tested 278 patients with positive amyloid and found that