This study demonstrates several aspects of the evolution of clinical trial methodologies to assess potentially disease-modifying agents in patients with neurodegenerative disorders.
These observations suggest that the expression of astrocyte connexins varies during the progression of this neurodegenerative disease.
Recent years have seen the identification of many genetic defects that underlie hereditary neurodegenerative disorders in humans.
Microglia have been implicated in aging-related neurodegenerative disease, yet relatively little is known about how normal aging and chronic pathological states may affect microglial function.
Consequently, insulin abnormalities may disrupt normal memory functioning and promote pathophysiological processes observed in patients with neurodegenerative disorders.
Potentially reversible impairments are likely to precede the neurodegenerative changes that characterize dementia.
Excitotoxicity appears to play a role in both neurodegenerative and cerebrovascular diseases.
There is substantial evidence that such reactive and inflammatory responses make significant contributions to neuronal damage in neurodegenerative diseases.
