A drug currently approved by the FDA for the treatment of dry mouth in Sjogren's syndrome (an autoimmune disease that affects excorine glands) has been shown to reduce levels of amyloid-β (Aβ) peptide in the cerebral spinal fluid of Alzheimer's patients-the first drug ever shown to have such an effect in human patients. Aβ peptide accumulates in the brain into the plaques that are a hallmark of Alzheimer's, and is a leading suspected cause of the disease. The compound AF102B, a selective activator of the M1 muscarinic receptor, blocks production of Aβ by increasing the activity of α-secretase and possibly also by inhibiting γ-secretase. The drug was therefore tested in 19 Alzheimer patients and found to reduce CSF Aβ levels by 22% in 14 patients. The drug is now in a Phase II trial that will assess its effects of cognitive status and long-term disease progression.—Hakon Heimer


  1. First good evidence that the in vitro effects of muscarinic stimulation can be seen physiologically.

    View all comments by Edward Koo

Make a Comment

To make a comment you must login or register.


No Available References

Further Reading

No Available Further Reading

Primary Papers

  1. . The selective muscarinic M1 agonist AF102B decreases levels of total Abeta in cerebrospinal fluid of patients with Alzheimer's disease. Ann Neurol. 2000 Dec;48(6):913-8. PubMed.