There is no single best treatment for Alzheimer’s disease. The most effective approach depends on the stage of the disease, and for most people it combines medication with lifestyle changes that protect remaining brain function. For those diagnosed early enough, newer drugs that target the underlying biology of Alzheimer’s can slow cognitive decline by roughly 27 to 33%, while older medications help manage symptoms at every stage.
Newer Drugs That Slow the Disease
The biggest shift in Alzheimer’s treatment has come from a new class of infusion-based drugs that clear amyloid plaques from the brain. Two are currently approved and in clinical use: lecanemab (sold as Leqembi) and donanemab (sold as Kisunla). Both target early-stage Alzheimer’s, meaning they’re designed for people with mild cognitive impairment or mild dementia, not advanced disease.
In large clinical trials, lecanemab slowed cognitive decline by about 27% compared to a placebo. Donanemab performed slightly better in its ideal group of participants, slowing decline by roughly 33%. These numbers are meaningful but modest. The drugs don’t stop or reverse the disease. They buy time, keeping people closer to their baseline abilities for longer.
Both drugs work by helping the immune system clear the sticky amyloid protein that builds up between brain cells in Alzheimer’s. They’re given as intravenous infusions, typically every two to four weeks, and require regular MRI monitoring throughout treatment. Donanemab has a potential advantage in that some patients can stop treatment once their amyloid levels drop below a certain threshold, rather than continuing indefinitely.
Who Qualifies for These Treatments
You can’t simply request these drugs. Before starting treatment, your doctor must confirm that amyloid plaques are actually present in your brain. This used to require either a PET scan or a lumbar puncture to collect spinal fluid, both of which are expensive or uncomfortable. Newer blood tests can now detect amyloid and are becoming part of the diagnostic toolkit, though they’re typically used alongside imaging rather than as a standalone confirmation.
You also need a diagnosis of either mild cognitive impairment due to Alzheimer’s or mild dementia due to Alzheimer’s. People with moderate or advanced dementia don’t qualify based on current evidence, since the trials only enrolled early-stage patients. In Europe, there’s an additional restriction: these drugs are limited to people who carry either zero or one copy of a gene variant called APOE ε4. People with two copies of that variant face higher risks of side effects.
Risks of Anti-Amyloid Drugs
The most significant side effect of both lecanemab and donanemab is a set of brain changes known as amyloid-related imaging abnormalities, or ARIA. These show up on MRI as either brain swelling or tiny areas of bleeding. Across clinical trials of anti-amyloid drugs, about one in four patients developed brain swelling on imaging, though many had no symptoms. Roughly 7% experienced symptoms like headache, confusion, or dizziness, and about 3.5% had severe episodes. Small brain bleeds appeared in about 18% of patients.
Most ARIA episodes resolve on their own, but they require close monitoring. This is why regular MRI scans are part of the treatment protocol, adding both time and cost to the process.
Cost and Medicare Coverage
Medicare covers FDA-approved anti-amyloid drugs, but with conditions. Your provider must confirm amyloid pathology and an early-stage diagnosis, and they must participate in a qualifying study or registry that collects real-world data on how well these treatments work. If you meet the criteria, you pay 20% of the Medicare-approved amount after meeting your Part B deductible. The scans and tests required before and during treatment add to out-of-pocket costs. If you don’t meet Part B coverage criteria, your Part D prescription plan may offer an alternative path to coverage.
Medications That Manage Symptoms
The older, more established Alzheimer’s drugs don’t slow the underlying disease, but they help the brain work more efficiently with what it has. Cholinesterase inhibitors boost levels of a chemical messenger called acetylcholine, which brain cells use to communicate and which declines as Alzheimer’s progresses. Three versions are available: donepezil, rivastigmine, and galantamine.
A long-term study published in Neurology found that all three were associated with slightly higher cognitive scores over time compared to nonusers. Galantamine showed the largest effect, improving scores by about 0.18 points per year on a standard cognitive test. That’s a small number on paper, but over several years it can translate to noticeably better day-to-day function. Galantamine also has a unique mechanism: it enhances the activity of nicotinic receptors in the brain in addition to preserving acetylcholine, which may explain its edge.
Memantine works differently. Instead of boosting acetylcholine, it regulates a different signaling system that can become overactive in Alzheimer’s and damage brain cells. It’s typically used in moderate to severe stages, sometimes in combination with a cholinesterase inhibitor. These drugs remain the backbone of treatment for people who don’t qualify for the newer therapies or who have progressed beyond the early stage.
Exercise and Physical Activity
Among non-drug approaches, physical activity has the strongest evidence. Observational studies consistently show that people who exercise regularly are less likely to develop dementia, with the strongest data pointing to midlife physical activity as protective against late-life cognitive decline. But exercise also matters after a diagnosis. It improves blood flow to the brain, stimulates the growth of new brain cells in memory-related areas, reduces inflammation, and releases compounds that support overall brain function.
The threshold is lower than many people expect. Walking at least 30 minutes a day at a moderate pace is supported by the epidemiological evidence. Aerobic exercise that raises your heart rate offers additional benefits, and there’s growing evidence that strength training helps too. Even very elderly and frail adults can start a new exercise routine and see benefits, so it’s never too late to begin.
Diet, Social Activity, and Mental Stimulation
The MIND diet, a hybrid of Mediterranean and heart-healthy dietary patterns, has early evidence suggesting it may help prevent memory loss. It emphasizes leafy greens, berries, nuts, whole grains, fish, and olive oil while limiting red meat, butter, cheese, and fried foods. The evidence is more about prevention than treatment, but nutritional quality supports brain health at any stage.
Cognitive stimulation, things like crossword puzzles, reading, Sudoku, learning new skills, and volunteer work, may strengthen the brain’s existing neural circuits. Education and lifelong learning are consistently linked to lower dementia risk in large population studies. The effects of cognitive activities after diagnosis appear relatively small in clinical research, but they carry no risk and contribute to quality of life. Volunteer work is particularly interesting because it combines mental challenge with social engagement, which independently supports cognitive health.
Putting It Together
For someone in the early stages of Alzheimer’s, the current best approach is a combination: an anti-amyloid drug if eligible, a cholinesterase inhibitor for symptom management, regular physical activity, a brain-healthy diet, and sustained mental and social engagement. For those in moderate or later stages who don’t qualify for the newer drugs, cholinesterase inhibitors and memantine remain the pharmacological options, and lifestyle interventions still contribute meaningfully to quality of life and daily function. The treatment landscape has changed substantially in the past few years, and the options available today offer more than symptom management alone for the first time in the history of the disease.