LET'S DO LUNCH ... The La Comida Lunch Program for Seniors has been serving nutritious and affordable hot lunches to seniors 60-plus since 1972. Diners enjoy a complete three-course meal served Monday through Friday from 11:15 a.m. to 12:15 p.m. Cost is a "suggested contribution" of $3. The lunches allow for socializing in a cheerful, friendly setting, sometimes with live musical entertainment. The dining room is in downtown Palo Alto at 450 Bryant St., inside the Avenidas building. For more information and current menus visit www.lacomida.org or call 650-322-3742.
ABOUT CAREGIVING ... A series of free seminars for caregivers is underway at the Stanford Health Library addressing topics such as handling isolation, the evolution of living with an illness, a shifting sense of self and managing emotions and finances. The first two seminars, given in September, were filled to capacity of 50 attendees. But space is still available for seminars Nov. 7 ("I Can't Do It All — Getting Help Caring for a Loved One") as well as seminars Nov. 21 ("Where Will the Money Come From? Navigating the Legal and Financial Aspects of Caregiving") and Jan. 9 ("At the End of the Day, How Can I Care for Myself? Identifying Resources and Coping Skills for Healthcare Professionals"). The sessions are cosponsored by the Stanford Health Library, Stanford Hospital and Clinics, Stanford Cancer Institute and the Fremont-based Cancer Prevention Institute of California. The Thursday, 7 to 9 p.m. sessions are at the Health Library, located in the Hoover Pavilion near Stanford Shopping Center at 211 Quarry Road, Suite 201. Reservations are required. Call 650-498-7826 or go to email@example.com.
NEW ALZHEIMER'S FINDING ... Scientists at Stanford University School of Medicine have shown how a protein fragment known as beta-amyloid, strongly implicated in Alzheimer's disease, begins destroying synapses before it clumps into plaques that lead to nerve cell death. Key features of Alzheimer's, which affects about 5 million Americans, are wholesale loss of synapses — contact points by which nerve cells relay signals to one another — and a parallel deterioration in brain function, notably in the ability to remember. "Our discovery suggests that Alzheimer's disease starts to manifest long before plaque formation becomes evident," said Carla Shatz, professor of neurobiology and of biology and senior author of the study, published Sept. 20 in the journal "Science." Using an experimental mouse strain that is highly susceptible to the synaptic and cognitive impairments of Alzheimer's disease, Shatz and her colleagues showed that if these mice lacked a surface protein ordinarily situated very close to synapses, they were resistant to the memory breakdown and synapse loss associated with the disorder. The study demonstrated for the first time that this protein, called PirB, is a high-affinity receptor for beta-amyloid in its "soluble cluster" form, meaning that soluble beta-amyloid clusters stick to PirB quite powerfully. That trips off a cascade of biochemical activities culminating in the destruction of synapses.