Can Dementia Be Treated? What the Medications Actually Do

Age Brightly Blog | Dementia Series, Part 3 of 5 Featuring Dr. Cheryl Johnson, Lead Geriatrician at Age Brightly

One of the most persistent — and most harmful — myths about dementia is that nothing can be done about it.

It's simply not true. And as new treatments emerge, the window for meaningful intervention is getting wider.

Here's an honest picture of where treatment stands right now, and what's coming.

The current standard: cholinesterase inhibitors

For Alzheimer's and Lewy body dementia, the main drug treatments available in New Zealand are donepezil (a tablet) and rivastigmine (a patch). Both belong to a class called cholinesterase inhibitors, which work by increasing the availability of a neurotransmitter that helps damaged neurons function better — essentially helping the brain work more effectively despite the disease process happening within it.

Dr. Johnson is clear about what these medications can and can't do: "They stabilize or improve functional ability." They're not a cure, and they don't reverse the underlying disease. But keeping someone able to manage their daily life — and stay in their own home — is no small thing.

Who do they help?

For people with Alzheimer's living at home (not yet in residential care), Dr. Johnson uses a simple framework to set expectations with patients and families:

• One in three people don't respond — they continue to decline at the same rate
• One in three stay about the same — which is considered a good outcome
• One in three improve — sometimes significantly

"Better can be really varied," she says. "Some people say their memory's better, they're coping better, they're less angry, less frustrated, they're sleeping better, they've got more get up and go."

That's two out of three people experiencing some benefit.

For Lewy body dementia, the numbers are even more encouraging — response rates of 70–80%, which Dr. Johnson says is actually higher than for Alzheimer's. Interestingly, clinicians had observed this for years before the research caught up to confirm it.

What about side effects?

This is where it gets more complicated. Around 20–30% of people experience side effects significant enough to stop the medication. These include nausea, diarrhoea, appetite loss, weight loss, and occasionally confusion.

To minimise this, Dr. Johnson typically prescribes donepezil at night — so any nausea happens during sleep rather than through the day. If gut symptoms become a problem on the tablet, switching to the rivastigmine patch (which bypasses the digestive system) can make a significant difference.

Dosing also follows the geriatric principle of "start low, go slow" — beginning at the lowest effective dose and increasing gradually over six to eight weeks, watching closely for side effects along the way.

The medication that's changing everything: lecanemab

This is where Dr. Johnson's measured optimism becomes something more. "I'm really excited by this," she says — a notable statement from someone in a field that deals with a lot of hard news.

Lecanemab is a biological therapy — an anti-amyloid treatment that doesn't just manage symptoms but actively targets and clears the amyloid protein responsible for Alzheimer's. It's been approved by the FDA in the United States, is available in the UK, and is working its way toward Australia. New Zealand tends to move more slowly on funding approvals, but the direction of travel is clear.

There are two things that make lecanemab genuinely significant:

First, it can be used in mild cognitive impairment and early Alzheimer's — stages where the existing medications don't actually change outcomes. For people caught early, this is a treatment that wasn't previously available to them.

Second, it only works if it's used early. If the disease has progressed to mid or late stages, the window has closed.

"This is why really early diagnosis is really important," Dr. Johnson says. "We've got to pick you up early."

The case for knowing sooner

The emergence of lecanemab makes early diagnosis not just useful but potentially decisive. The protein changes that lead to Alzheimer's begin accumulating 10–20 years before symptoms appear. Scans that detect amyloid in the brain are available in the private sector now.

"It's really going to change what we do," says Dr. Johnson. "Having access to these scans, showing that someone's got amyloid — we're going to have to start thinking about who we treat, and really trying to prevent people getting into the mild cognitive impairment group in the first place."

More on early diagnosis — and what's getting in the way of it — in Part 4.

Next in the series: Why it takes an average of three and a half years to get a dementia diagnosis in New Zealand — and what we can do about it.