ABSTRACT
Higgins (1992) stated that amyloid deposition
is at the core of AD pathology and that the
other pathophysiological features of AD
including the accumulation of highly
phosphorylated tau in neurofibrillary tangles
in neurons, the loss of neurons and the
subsequent atrophy and clinical symptoms, all
result as a consequence of amyloid deposition.
The amyloid cascade hypothesis has had some
modifications – it may be intercellular amyloid
that is important and it may be necessary for
