The sources of A[beta] accumulated in
senile plaques are known to be multiple.
The
senile plaques and neurofibrillary tangles are involved in damaging the neurons, but the exact mechanisms of their action are still largely unknown.
There has been some debate as to whether targeting Ap would be sufficient for an immunologically based therapy, because the role of
senile plaques in the clinical picture appears to be just the tip of the iceberg.
This may be due to glucose dysregulation, accumulation of
senile plaques, metabolic oxidation products associated with hyperglycemia, insufficient action or effect of insulin due to insufficient secretion, activity, or both, neuronal damage as a result of advanced glycosylated end-product production and oxidative stress, damage to vascular endothelium as a result of high osmotic stress induced by hyperglycemia which disrupts the blood-brain barrier causing local leakage of vascular substances and aggravates neuronal damage.
DSCAM immunoreactivity has been found in the core of
senile plaques and in surrounding synapses, suggesting some role for DSCAM in plaque formation (16).
AD is the most common senile dementia due to the formation of
senile plaques and neurofibrillary tangles.
(1979) Dementia Parkinsonism syndrome with numerous Lewy bodies and
senile plaques in cerebral cortex.
Grimm said studies have already shown that cholesterol promotes the formation of so-called
senile plaques. These plaques, which are composed of proteins, particularly beta-amyloid proteins, deposit at nerve cells within the brain and are regarded as one of the main causes of Alzheimer's disease.
Unlike most mental disorders, neuropathological changes associated with AD represented by neurofibrillary tangles and
senile plaques, were identified at the outset.