For almost all of us, the risk of getting Alzheimer’s depends on our age more than anything else.

That’s because Alzheimer’s is primarily a disease of aging — even if most researchers don’t approach it that way.

Perhaps they should.

A leading authority on dementia research says we might see effective treatments sooner if we put more focus on how the chronic conditions of aging contribute to Alzheimer’s and develop medicines that target those conditions.

Dr. Howard Fillit says that strategy has worked on other age-related illnesses — including heart disease, cancer and hypertension — and the time has come to attack Alzheimer’s that way.

“The overarching idea here is that the leading risk factor for Alzheimer’s disease is aging,” says Fillit, founding executive director and chief science officer of the Alzheimer’s Drug Discovery Foundation. “What hasn’t been done, and what we’ve been working to do for a very long time now, is bring to (Alzheimer’s) research the concepts of biological gerontology that are common to almost all diseases of aging.”

Fillit makes that case in a research review published last month in the online issue of the journal Neurology. In his paper, he says novel approaches that tackle the effects of aging on the brain could usher in a “new generation” of medicines to prevent and treat Alzheimer’s.

These therapies might aim at such condition as inflammation or oxidative stress, Fillit says.

“In 1995, more than 20 years ago, I showed that people with Alzheimer’s disease had evidence of increased inflammation in their blood,” Fillit says. “Inflammation is a hallmark of aging, but we haven’t applied the knowledge that’s been gained over almost 70 years now about aging and used it to develop new drugs to treat Alzheimer’s disease.”

Why not?

Well, part of the reason is that researchers became enamored with other approaches — ones that so far haven’t been fruitful.

Fillit traces that back to the mid-1980s, when the presence of beta-amyloid “plaques” in the brain of Alzheimer’s patients was first identified as a tell-tale sign of the disease.

“That’s why, historically, beta-amyloid has been the primary target for new drugs, because it was the first clue we had to what was going on,” Fillit says. “Ever since then, we’ve been trying to target that protein.”

In his article in Neurology, Fillit notes that more than half of the more advanced clinical trials currently underway target either the amyloid plaques, or the “tangles” of tau protein that are another hallmark of Alzheimer’s. He says these approaches looked promising in preliminary studies, but so far have been “largely unsuccessful’’ in slowing or halting the progression of Alzheimer’s.

“Pathology doesn’t necessarily mean these are good drug targets, and so far they haven’t been,” Fillit says. “Getting rid of the plaques and tangles doesn’t necessarily mean that’s going to help.”

That unproductive emphasis on plaques and tangles is one reason there has not been a major breakthrough in Alzheimer’s drug research in well over a decade.

Fillit has not given up on what’s called the “amyloid hypothesis,” and says it may eventually prove to be part of the solution. But his organization, the Alzheimer’s Drug Discovery Foundation, has been working for years to broaden and diversify the research efforts, including an emphasis on drugs that target the biology of aging.

The concept of Alzheimer’s as a disease of aging is supported by the statistics. Most cases of the disease are what’s called late-onset Alzheimer’s, and the average age of onset is 75. Beginning around the age of 65, your risk of Alzheimer’s goes up about 2 percent every year. By the age of 85, the risk of Alzheimer’s is around 50 percent for the average American.

Fillit says research already is gravitating toward the kinds of health concerns that arise in the aging process.

“There are more clinical trials out there targeting the mechanisms of aging that are relevant to Alzheimer’s disease,” he says. “They are not targeted at beta-amyloid and tau, but toward other things. There are about 40 different trials going on now that target these non-amyloid, non-tau approaches.”

Pursuing a variety of medications is important, because Fillit and other Alzheimer’s experts do not believe the disease will be conquered by a single blockbuster drug. Instead, they foresee it being treated with some combination of medications, in addition to improvements in health habits, the way such conditions as AIDS and heart disease are.

“We think that we’re going to need combinations of therapies because aging is a very complex biology and Alzheimer’s is a complex biology,” Fillit says. “People who have cancer, which is predominantly a disease of aging, are on three, four or even five different drugs. With diabetes, they are often on two or three different drugs. All of these chronic diseases of old age require combination therapies to attack the multiple mechanisms that affect the brain and cause Alzheimer’s disease.”

Fillit says the chronic conditions of aging that can be associated with Alzheimer’s include not just inflammation, but also metabolic dysfunction, vascular problems and loss of synapses in the brain.

There are many avenues for Alzheimer’s research to target the risk factors of aging. One that the Alzheimer’s Drug Discovery Foundation supports is the practice of “repurposing” drugs. That involves taking a medication that’s been proven to treat some other illness and applying it to Alzheimer’s.

One example would be a drug called AGB101, which is being tested on people with a mild form of memory loss to see if it can prevent them from progressing to Alzheimer’s, or at least delay the progression.

AGB101 is a low-dose version of levetiracetam, a drug that has been used to treat epilepsy for more than a decade. It does not target plaques or tangles. Instead, it is being tested to see if it can preserve memory and delay cognitive decline by preventing the hyperactive firing of neurons in the brain of people who have signs of Alzheimer’s disease. That hyperactivity is believe to hasten memory loss.

In a small study, the drug not only proved to be safe, but significantly improved memory in a group of several dozen older adults.

Last week, the maker of the drug, AgeneBio, announced that it has enrolled the first patients in a Phase 3 clinical trial that eventually will involve more than 800 patients at study sites across the United States, Canada and Europe.

Sharon Rosenzweig-Lipson, AgeneBio research and development vice-president, said the company is “pleased to be at the forefront of a new direction in Alzheimer’s disease research moving beyond amyloid-directed therapeutics.”

Fillit says one of the great advantages of repurposing a drug already approved by the FDA for other conditions is that if it proves effective against Alzheimer’s, it can immediately be used for that purpose.

“If any of these trials are successful, doctors don’t have to wait for an FDA approval years down the road to enable patients to have access to the drug,” he says. “We can prescribe that drug right away as an ‘off-label’ drug.”

It’s opportunities like these that have Fillit excited about the future of Alzheimer’s research. He’s been studying Alzheimer’s for 40 years and treating Alzheimer’s patients for nearly that long, and he says the potential for a cure has never looked more promising.

“I just want to express complete optimism about where we are and where we’re going,” he says. “I’m very optimistic that we will have in the relatively near future, three to five years, some drugs on the market that will be effective and safe for the treatment of Alzheimer’s, and we also know a lot about the prevention of Alzheimer’s today, so I’m very excited and optimistic about where we are.”

Tony Dearing may be reached at tdearing@njadvancemedia.com. Follow him on Twitter @TonyDearing. Find NJ.com on Facebook.