Sandbox Reserved 591: Difference between revisions

From Proteopedia
Jump to navigationJump to search
Student (talk | contribs)
No edit summary
Student (talk | contribs)
No edit summary
Line 13: Line 13:
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. These peptides are deposited as amyloid plaques in the brains of AD individuals.  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. It is suggested that disturbance of normal APP phisiology can conribute to the development of AD. <ref>PMID:3210295</ref>.[[Image:nihms319849f1.jpg|thumb|left|350px|Alzheimer's disease]]
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. These peptides are deposited as amyloid plaques in the brains of AD individuals.  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. It is suggested that disturbance of normal APP phisiology can conribute to the development of AD. <ref>PMID:3210295</ref>.[[Image:nihms319849f1.jpg|thumb|left|350px|Pathology of Alzheimer's disease. Brain sections from a patient show plaques on the neurites.]]
==References==
==References==
'<references/>'
'<references/>'