Tumor necrosis factor α (TNF-α) plays a central role in the pathophysiology of Alzheimer’s disease (AD). Food and Drug Administration–approved biologic TNF-α inhibitors are thus a potential treatment for AD, but they do not cross the blood-brain barrier. In this short review, we discuss the involvement of TNF-α in AD, challenges associated with the development of existing biologic TNF-α inhibitors for AD, and potential therapeutic strategies for targeting TNF-α for AD therapy.

By JACEP Open policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article as per ICMJE conflict of interest guidelines (see www.icmje.org). The authors have stated that no such relationships exist.

The naevoid basal cell carcinoma syndrome (NBCCS; Gorlin's Syndrome) was first fully described by Gorlin and Goltz in 1960 and consists of the classic triad of multiple basal cell carcinomas, odontogenic keratocysts and skeletal anomalies (Gorlin & Goltz, 1960; Gorlin, 1987). Osteosclerotic foci are a rare feature of this condition (Hermann & Som, 1981; Blinder et al, 1984) and we present a case in which bone scintigraphy proved helpful in excluding presumed metastatic disease as a cause of these sclerotic lesions. A 46-year-old woman on follow-up for NBCCS complained of 2 months low back pain and sciatica in February 1990. Lumbosacral and pelvic radiographs, obtained at the time, showed multiple sclerotic foci within the pelvis (Figure 1) and lumbar vertebral bodies (Figure 2). A presumptive diagnosis of multiple metastases was made and the patient referred for further assessment.

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