Sandbox Reserved 591: Difference between revisions
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resulted in a growth of synaptic size and improved memory capabilities in animals. An RHDS motif at the C-terminius of APP seems to promote cell adhesion. Experimental evidence has determined that APP controls the presynaptic expression and action of the high affinity choline transporter. In this circumstance, loss of APP leads to abnormal positioning of the choline transporter at neuromuscular junctions which could results in cholinergic impairment and AD pathogenesis. | resulted in a growth of synaptic size and improved memory capabilities in animals. An RHDS motif at the C-terminius of APP seems to promote cell adhesion. Experimental evidence has determined that APP controls the presynaptic expression and action of the high affinity choline transporter. In this circumstance, loss of APP leads to abnormal positioning of the choline transporter at neuromuscular junctions which could results in cholinergic impairment and AD pathogenesis. | ||
== Clinical Relevance == | == Clinical Relevance == | ||
Alzheimer's disease (AD) is the leading cause of dementia throughout the world which is characterized by the accumulation of β-Amyloid peptide (Aβ) within the brain. It affects one out of three individuals in elder people. These peptides are deposited as amyloid plaques in the brains of AD individuals. Researchers are trying to figure out ways to keep these plaques from forming because of majority of them believe that these plaques are responsible for the pathology of AD. Research suggests that the generation of Aβ from APP proteolysis is a crucial step in the development of AD. Aβ also leads to the neurodegenerative conditions seen in AD. <ref>Zhi-dong Zhou. 2011. The roles of amyloid precursor protein (APP) in neurogenesis, implications to pathogenesis and therapy of Alzheimer disease (AD). PMC 5(4): 280–92.</ref>. It is suggested that disturbance of normal APP physiology can contribute to the development of AD. Even though no cure currently exists for AD, significant progress has been made in developing treatments for it. <ref>PMID:3210295</ref>. Future treatments are likely to include drugs that target steps in Aβ production. <ref>PMID: | Alzheimer's disease (AD) is the leading cause of dementia throughout the world which is characterized by the accumulation of β-Amyloid peptide (Aβ) within the brain. It affects one out of three individuals in elder people. These peptides are deposited as amyloid plaques in the brains of AD individuals. Researchers are trying to figure out ways to keep these plaques from forming because of majority of them believe that these plaques are responsible for the pathology of AD. Research suggests that the generation of Aβ from APP proteolysis is a crucial step in the development of AD. Aβ also leads to the neurodegenerative conditions seen in AD. <ref>Zhi-dong Zhou. 2011. The roles of amyloid precursor protein (APP) in neurogenesis, implications to pathogenesis and therapy of Alzheimer disease (AD). PMC 5(4): 280–92.</ref>. It is suggested that disturbance of normal APP physiology can contribute to the development of AD. Even though no cure currently exists for AD, significant progress has been made in developing treatments for it. <ref>PMID:3210295</ref>. Future treatments are likely to include drugs that target steps in Aβ production. <ref>PMID: | ||
3210295</ref>. [[Image:nihms319849f1.jpg|thumb|left|350px|''Figure 2'' Pathology of Alzheimer's disease. Brain sections from a patient show plaques on the neurites.]] | |||
==References== | ==References== | ||
'<references/>' | '<references/>' | ||
