We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure [email protected]
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The amyloid hypothesis has been the dominant theory for the cause of Alzheimer’s disease for over 20 years. In brief, the theory holds that Alzheimer’s disease is caused by the accumulation of beta-amyloid that damages nerve cells in the brain. Beta-amyloid is cleaved from the large amyloid precursor protein (APP) into two main peptides that are released outside the cell, beta-amyloid 40 and beta-amyloid 42, containing respectively 40 and 42 amino acids. According to the amyloid hypothesis, in normal people, these peptides are rapidly removed, but in people with Alzheimer’s disease the metabolic ability to degrade them is decreased, the peptides accumulate, form fibrils, and ultimately solid amyloid plaques that in turn damage neurons and trigger the formation of abnormal tau pathology causing neuronal death.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.