You might think age-related dementia has been with us all along, stretching back to the ancient world.

But a new analysis of classical Greek and Roman medical texts suggests that severe memory loss — occurring at epidemic levels today — was extremely rare 2,000 to 2,500 years ago, in the time of Aristotle, Galen and Pliny the Elder.

The USC-led research, published in the Journal of Alzheimer’s Disease, bolsters the idea that Alzheimer’s disease and related dementias are diseases of modern environments and lifestyles, with sedentary behavior and exposure to air pollution largely to blame.

“The ancient Greeks had very, very few — but we found them — mentions of something that would be like mild cognitive impairment,” said first author Caleb Finch, a University Professor at the USC Leonard Davis School of Gerontology. “When we got to the Romans, and we uncovered at least four statements that suggest rare cases of advanced dementia — we can’t tell if it’s Alzheimer’s. So, there was a progression going from the ancient Greeks to the Romans.”

Do we see Alzheimer’s in history?

Ancient Greeks recognized that aging commonly brought memory issues we would recognize as mild cognitive impairment, or MCI, but nothing approaching a major loss of memory, speech and reasoning as caused by Alzheimer’s and other types of dementia.

Finch and co-author Stanley Burstein, a historian at California State University, Los Angeles, pored over a major body of ancient medical writing by Hippocrates and his followers. The text catalogs ailments of the elderly such as deafness, dizziness and digestive disorders — but makes no mention of memory loss.

Centuries later in ancient Rome, a few mentions crop up. Galen remarks that at the age of 80, some elderly begin to have difficulty learning new things. Pliny the Elder notes that the senator and famous orator Valerius Messalla Corvinus forgot his own name. Cicero prudently observed that “elderly silliness … is characteristic of irresponsible old men, but not of all old men.”

Finch speculates that as Roman cities grew denser, pollution increased, driving up cases of cognitive decline. In addition, Roman aristocrats used lead cooking vessels, lead water pipes and even added lead acetate into their wine to sweeten it — unwittingly poisoning themselves with the powerful neurotoxin.

(A few ancient writers recognized the toxicity of lead-containing material, but little progress was made in dealing with the problem until well into the 20th century. Some scholars blame lead poisoning for the fall of the Roman Empire.)

For this paper, Finch did not just think about the Roman Empire or the Greeks. In the absence of demographic data for ancient Greece and Rome, Finch turned to a surprising model for ancient aging: today’s Tsimane Amerindians, an Indigenous people of the Bolivian Amazon.

Alzheimer’s in history: Look at the Tsimane

The Tsimane — like the ancient Greeks and Romans — have a preindustrial lifestyle that is very physically active, and they have extremely low rates of dementia. An international team of cognitive researchers led by Margaret Gatz, a professor of psychology, gerontology and preventive medicine at the USC Leonard Davis School, found among older Tsimane people, only about 1% suffer from dementia. In contrast, 11% of people aged 65 and older living in the United States have dementia, according to the Alzheimer’s Association.

“The Tsimane data, which is quite deep, is very valuable,” Finch said. “This is the best-documented large population of older people that have minimal dementia, all of which indicates that the environment is a huge determinant on dementia risk. They give us a template for asking these questions.”

The paper was supported by funds from the Cure Alzheimer’s Fund and the National Institutes of Health (P01 AG055367 and R01 AG05442).

An Alzheimer’s diagnosis in a sibling raises the risk of a shortened lifespan in other family members — even those without dementia, according to new USC research based on data from the Swedish Twin Registry.

The study, published Monday in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, suggests that the same combination of genetics and environment — nature plus nurture — that shortens longevity in someone with dementia may also shorten the life of siblings without dementia.

“We expected a different result. We expected that, in twins where one developed dementia and the other did not, the difference in lifespan would be just like we see in unrelated people,” said lead author Jung Yun Jang, who conducted the research as part of her doctoral studies in clinical science in the Department of Psychology at the USC Dornsife College of Letters, Arts and Sciences.

“We assumed the reason a person who has developed dementia has a shortened life expectancy is because the dementia leads to other medical conditions that affect mortality,” Jang said. “What we’re seeing instead is the increased risk of mortality is not due to just the dementia itself, but also a whole package of other influences that the person brings to their disease.”

In addition to Jang, other authors include Margaret Gatz, a professor of psychology, gerontology and preventive medicine at USC Dornsife; Christopher Beam, an assistant professor of psychology and gerontology at USC Dornsife; and Ida Karlsson and Nancy Pedersen of the Karolinska Institutet in Sweden.

Alzheimer’s lifespan: Longevity affected in siblings with — and without — dementia

The new study is part of Gatz and Pedersen’s landmark body of work on aging and cognition with the Swedish Twin Registry, a large cohort study of more than 45,000 Swedish twins. Across nearly 40 years, their collaborative work with twins — including genetically identical pairs — is designed to tease apart the roles of genes and environment.

Identical twins share 100% of their genotype; fraternal twins (and full siblings) share, on average, 50% of their genotype. Most twins — identical or fraternal — generally share the same rearing environment. That environment includes such factors as early life exposures to pollution, diet, education and physical activity.

This study included 90 pairs of identical twins and 288 pairs of fraternal twins, in which one twin had dementia while the other did not.

Jang confirmed that developing dementia affects longevity in a patient, and that people live for about seven years on average after a dementia diagnosis — a finding that has been confirmed in other studies.

Other findings included:

• In identical twins, when one is diagnosed with dementia, both twins have a similarly shortened life expectancy.
• In fraternal twins, when one is diagnosed with dementia, the twin who has not developed dementia has a slightly shortened life expectancy compared to someone who has no sibling with dementia.
• The research suggests that dementia itself is not the sole cause of a shortened lifespan, but instead a combination of shared genes and environment. Both twins may develop cardiovascular disease, for example, which can contribute to dementia in one and shortened lifespans in both.

“What happens early in the life course is really important,” Gatz said. “You may not be able to change that for yourself, but it does seem like the message to parents is, make sure your kid eats healthy, make sure your kid gets exercise, make sure your kid gets an education. You’re actually contributing to giving that kid a lower chance of developing dementia 75 years later.”

Jang said she was inspired to pursue the research because “one of the most frequently asked questions when a family member receives a diagnosis of dementia is: How much time do we have?”

Jang added, “We believed that asking this question in twins would inform patients and families in making their financial and end-of-life decisions as they deal with this disease that causes losses over time.”

The work was supported by grants from the National Institutes of Health (R01 AG060470 and T32 AG000037); the Swedish Research Council for Health, Working Life and Welfare; the Strategic Research Program in Epidemiology at Karolinska Institutet; Loo and Hans Osterman’s Foundation; Foundation for Geriatric Diseases at Karolinska Institutet; and Karolinska Institutet’s Research Foundation.