Alzheimer’s disease remains a significant health challenge, affecting about 10 percent of people over age 65 and causing more deaths annually than breast cancer and prostate cancer combined. The disease has long been difficult to diagnose and treat, but recent scientific advances are changing the landscape.
In the past two years, the U.S. Food and Drug Administration approved drugs that slow memory loss by targeting amyloid protein deposits in the brain. These treatments can delay cognitive decline by up to seven months but do not cure or reverse Alzheimer’s and may cause side effects.
“There is concern from some that these medicines are not as effective or as safe as desired for people with symptoms of Alzheimer’s,” said Adam Boxer, neurology professor at UC San Francisco. “But this is just the first generation.” He likened current Alzheimer’s medications to early HIV treatments, which improved significantly over time. Boxer is leading a five-year clinical trial funded by the National Institutes of Health that combines anti-amyloid drugs with therapies targeting tau proteins, another hallmark of Alzheimer’s pathology. “The thought is that a combination of an anti-amyloid and an anti-tau drug could have a much larger effect than either alone,” he said.
Another area of research focuses on restoring cognitive function after damage has occurred. Istvan Mody, professor at UCLA Health, explained: “The hope with the anti-amyloid drugs was that with the removal of the plaques, the disease would be cured. Unfortunately, that hasn’t been the case. The removal of these toxic compounds still leaves an altered brain behind.” Mody’s team discovered a molecule that increases gamma oscillations—brain signals associated with memory—which restored maze navigation abilities in mice with Alzheimer’s disease. “We’ve shown that this works in mice,” Mody said. “If we can develop a therapy that’s safe and effective for people, we may be able to restore cognitive function. That’s the ultimate hope.”
Diagnosis methods are also improving rapidly. In May, the FDA approved its first blood test for diagnosing Alzheimer’s by detecting forms of tau and amyloid proteins in patients showing dementia symptoms. Researchers such as Hector M. González at UC San Diego have identified additional blood markers like NfL (a nerve cell injury marker) that could predict cognitive decline even before symptoms appear.
Preventive strategies are gaining attention as well. Rachel Whitmer at UC Davis noted: “The good news is, we now know that 45 percent of the overall population risk of dementia is accounted for by modifiable factors, like midlife hypertension, low social engagement, untreated hearing loss or hyperlipidemia, or exposure to air pollution.” Whitmer leads research showing cardiometabolic health improvements can reduce dementia risk from adolescence onward. She also heads UC Davis’s involvement in a national study where intensive lifestyle interventions led to higher cognitive scores among participants at risk for dementia.
On a molecular level, Martin Kampmann at UC San Francisco uses CRISPR gene editing—technology developed at UC Berkeley—to investigate genetic triggers for dementia by altering genes in cultured brain cells derived from patients’ skin or blood samples. This work helps identify how different gene states affect neuron survival and inflammation in the brain and points toward new drug targets beyond existing amyloid-focused therapies.
University of California campuses play a leading role in this field: they host eight out of ten California Alzheimer’s Disease Centers—a statewide network established four decades ago—and three serve as federally funded research centers specializing in Alzheimer’s studies.
However, continued progress depends on sustained federal funding for university research nationwide—a subject currently under debate in Congress.
