Neuropathic diagnosis of Alzheimer’s disease is typically based upon examination of the brain at autopsy and is determined by the number of plaques and tangles in the neurocortex (frontal, temporal, and parietal lobes), hippocampus and amygdala. A diagnosis of Alzheimer’s disease based upon neuropathologic criteria alone, however, is often difficult because there are a significant number of plaques and tangles in the neurocortex, hippocampus and amygdala of normal elderly people. In addition, the density of neocortical plaques and tangles has only a rough correlation with the degree of dementia. Perhaps the most alarming fact about diagnosis of Alzheimer’s disease is the fact that the only biochemically certain diagnosis depends on examination of a patient’s brain at autopsy.
Thus, diagnosis of Alzheimer’s disease in living patients depends on behavioral and more subjective medical criteria
Alzheimer’s disease has been difficult to diagnose and to treat. The discovery that levels of acetylcholinesterase are markedly reduced in the cortex and hippocampus of patients with Alzheimer’s disease has resulted in the development of a number of pharmaceutical compounds, which restore or replace cholinergic function. Examples of such compounds include tacrine (“THA”), physostigmine (an irreversible inhibitor of acetylcholinesterase) and physostigmine derivatives. In general, however, those compounds have met with only limited success.
Given the increasing number of individuals with Alzheimer’s disease, it is critical that new methods for diagnosing, treating and monitoring the disease be developed.
|
|
|
