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Enbrel May Help Treat Alzheimer’s
Rheumatoid Arthritis Drug May Prompt Rapid Improvement in Alzheimer’s Disease Symptoms
By Jennifer Warner
FROM THE WEBMD ARCHIVES
July 21, 2008 — A drug commonly used to treat rheumatoid arthritis and other immune-based conditions may also be effective at targeting language-related Alzheimer’s disease problems.
Disruption of language abilities, such as difficulty finding words to express thoughts, is a common symptom of Alzheimer’s disease.
A new study shows people with Alzheimer’s disease experienced rapid improvement in language abilities after treatment with Enbrel (etanercept). In fact, researchers videotaped noticeable language skill improvements in Alzheimer’s patients within minutes after receiving the drug.
The small, phase two clinical trial involved only 12 people with mild to moderate forms of Alzheimer’s disease, but researchers say the results merit further study in phase three clinical trials.
New Target for Alzheimer’s Disease Treatment
Etanercept works by targeting a substance produced by the immune system known as tumor necrosis factor-alpha (TNF-alpha). This substance is implicated in attacking healthy tissue and causing inflammation in people with immune system disorders, such as arthritis and certain skin conditions.
In the study, published in BMC Neurology, researchers treated 12 people with mild to moderate forms of Alzheimer’s disease weekly with Enbrel for six months. The drug is usually delivered by injection to the thigh, abdomen, or upper arm, but in this study researchers injected the drug into the muscles surrounding the spinal cord to deliver the drug directly to the nervous system and reduce TNF-alpha levels in the brain.
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The results showed improvements in conversational, naming, and comprehension abilities — and improvements in following spoken commands — began within minutes after injection.
Researchers say the findings may also offer new insight behind the development of Alzheimer’s disease and other forms of dementia and offer new avenues for treatment using immune-based therapies.
For example, researcher Edward Tobinick of the Institute for Neurological Research in Los Angeles and colleagues say elevated levels of TNF-alpha in the brain may interfere with the regulation of neural impulses controlling language in the brain. With further study, these effects may be reversible with drugs like etanercept that target TNF-alpha.
WebMD Health News
Reviewed by Brunilda Nazario, MD on July 21, 2008
Blood-Brain Barrier Penetrating Biologic TNF-α Inhibitor for Alzheimer's Disease. Chang R, et al. Mol Pharm. 2017.
Abstract
Tumor necrosis factor alpha (TNF-α) driven processes are involved at multiple stages of Alzheimer's disease (AD) pathophysiology and disease progression.
Biologic TNF-α inhibitors (TNFIs) are the most potent class of TNFIs but cannot be developed for AD since these macromolecules do not cross the blood-brain barrier (BBB). A BBB-penetrating TNFI was engineered by the fusion of the extracellular domain of the type II human TNF receptor (TNFR) to a chimeric monoclonal antibody (mAb) against the mouse transferrin receptor (TfR), designated as the cTfRMAb-TNFR fusion protein.
The cTfRMAb domain functions as a molecular Trojan horse, binding to the mouse TfR and ferrying the biologic TNFI across the BBB via receptor-mediated transcytosis.
The aim of the study was to examine the effect of this BBB-penetrating biologic TNFI in a mouse model of AD. Six-month-old APPswe, PSEN 1dE9 (APP/PS1) transgenic mice were treated with saline (n = 13), the cTfRMAb-TNFR fusion protein (n = 12), or etanercept (non-BBB-penetrating biologic TNFI; n = 11) 3 days per week intraperitoneally.
After 12 weeks of treatment, recognition memory was assessed using the novel object recognition task, mice were sacrificed, and brains were assessed for amyloid beta (Aβ) load, neuroinflammation, BBB damage, and cerebral microhemorrhages.
The cTfRMAb-TNFR fusion protein caused a significant reduction in brain Aβ burden (both Aβ peptide and plaque), neuroinflammatory marker ICAM-1, and a BBB disruption marker, parenchymal IgG, and improved recognition memory in the APP/PS1 mice. Fusion protein treatment resulted in low antidrug-antibody formation with no signs of either immune reaction or cerebral microhemorrhage development with chronic 12-week treatment.
Chronic treatment with the cTfRMAb-TNFR fusion protein, a BBB-penetrating biologic TNFI, offers therapeutic benefits by targeting Aβ pathology, neuroinflammation, and BBB-disruption, overall improving recognition memory in a transgenic mouse model of AD.
PMID 28514851 [Indexed for MEDLINE]