TFNa in autism, Alzheimer: Rapid cognitive improvement in Alzheimer's disease following perispinal etanercept administration

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<http://www.jneuroinflammation.com/content/5/1/2>*

Rapid cognitive improvement in Alzheimer's disease following perispinal

etanercept administration*

L. Tobinick, Hyman Gross

Journal of Neuroinflammation 2008, 5:2doi:10.1186/1742-2094-5-2

[Provisional PDF

<http://www.jneuroinflammation.com/content/pdf/1742-2094-5-2.pdf>]

Abstract (provisional)

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.

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*1: Pediatr Neurol. *2007 Jun;36(6):361-5.

*Elevation of tumor necrosis factor-alpha in cerebrospinal fluid of

autistic children.*

Chez MG, Dowling T, Patel PB, Khanna P, Kominsky M.

Department of Neurology, lind lin University, and the Chicago

Medical School, North Chicago, IL, USA. chezm2@...

Recent reports implicating elevated cytokines in the central nervous

system in a small number of patients studied with autism have reported

clinical regression. These studies have not focused on tumor necrosis

factor-alpha as a possible marker for inflammatory damage. A series of

10 children with autism had clinical evaluation of their serum and

spinal fluid for inflammatory changes and possible metabolic disease as

part of their neurological evaluation. Elevation of cerebrospinal fluid

levels of tumor necrosis factor-alpha was significantly higher (mean =

104.10 pg/mL) than concurrent serum levels (mean = 2.78 pg/mL) in all of

the patients studied. The ratio of the cerebrospinal fluid levels to

serum levels averaged 53.7:1. This ratio is significantly higher than

the elevations reported for other pathological states for which

cerebrospinal fluid and serum tumor necrosis factor-alpha levels have

been simultaneously measured. This observation may offer a unique

insight into central nervous system inflammatory mechanisms that may

contribute to the onset of autism and may serve as a potential clinical

marker. More controlled study of this potentially important observation

may prove valuable.

PMID: 17560496