Substantial basic science and clinical evidence suggests that excess
tumor necrosis factor-alpha (TNF-alpha) is centrally involved in the
pathogenesis of Alzheimer's disease. In addition to its pro-
inflammatory functions, TNF-alpha has recently been recognized to be a
gliotransmitter that regulates synaptic function in neural networks.
TNF-alpha has also recently been shown to mediate the disruption in
synaptic memory mechanisms, which is caused by beta-amyloid and beta-
amyloid oligomers. The efficacy of etanercept, a biologic antagonist
of TNF-alpha, delivered by perispinal administration, for treatment of
Alzheimer's disease over a period of six months has been previously
reported in a pilot study. This report details rapid cognitive
improvement, beginning within minutes, using this same anti-TNF
treatment modality, in a patient with late-onset Alzheimer's disease.
Rapid cognitive improvement following perispinal etanercept may be
related to amelioration of the effects of excess TNF-alpha on synaptic
mechanisms in Alzheimer's disease and provides a promising area for
additional investigation and therapeutic intervention.
Full text at:
http://www.jneuroinflammation.com/content/pdf/1742-2094-5-2.pdf