Alzheimer’s disease was first identified in 1901, making it a recognized medical condition for just over 120 years. But the underlying question is more interesting: did people get Alzheimer’s before anyone knew what to call it? The evidence suggests the disease existed in ancient times, though it was far rarer than it is today.
The Ancient World Had Very Little Dementia
A USC analysis of classical Greek and Roman medical texts found that severe memory loss, the kind we associate with Alzheimer’s and related dementias, was extremely rare 2,000 to 2,500 years ago. Hippocrates and his followers wrote extensively about ailments of aging, cataloging deafness, dizziness, and digestive problems, but made no mention of memory loss at all.
The ancient Greeks did recognize that aging commonly brought mild forgetfulness, something we’d now call mild cognitive impairment. But nothing in their writings approaches the devastating loss of memory, speech, and reasoning that defines Alzheimer’s. By the Roman period, a few scattered references to more serious cases appear. Galen noted that some people at age 80 began having difficulty learning new things. Pliny the Elder recorded that the senator Valerius Messalla Corvinus, a famous orator, forgot his own name. Cicero observed that “elderly silliness” was “characteristic of irresponsible old men, but not of all old men.”
That progression, from virtually no mentions in Greek texts to a handful of cases in Roman writings, is itself revealing. Researchers believe the difference reflects real changes in how people lived. Roman cities had higher population density, lead pipes, and more pollution. The researchers’ broader conclusion is striking: today’s epidemic levels of dementia likely stem in significant part from modern environments and lifestyles, not simply from people living longer.
The Disease Gets a Name: 1901 to 1910
The modern story of Alzheimer’s begins with a German psychiatrist named Alois Alzheimer. In 1901, he began treating Auguste Deter, a 51-year-old woman who displayed symptoms of memory loss, paranoia, and psychological changes. Her case was unusual because of her relatively young age and the severity of her decline.
After Deter died in 1906, Alzheimer performed a post-mortem examination of her brain and found two abnormalities that had never been formally described: dense deposits between nerve cells and tangled fibers inside them. We now call these beta-amyloid plaques and tau tangles, and they remain the defining biological hallmarks of the disease more than a century later.
Alzheimer presented his findings at a medical conference in 1906, but the condition didn’t yet have a name. That came in 1909, when the influential psychiatrist Emil Kraepelin included it as “Alzheimer’s disease” in his widely used psychiatric textbook. Kraepelin’s decision to name it after his colleague wasn’t based on a large body of evidence. Only a small number of cases had been documented. But the label stuck, and the disease entered the medical vocabulary for good.
Why It Took Decades to Understand
For most of the 20th century, Alzheimer’s disease was considered rare, something that struck people in their 50s and 60s. When older people lost their memories, doctors typically called it “senile dementia” and treated it as a normal part of aging rather than a disease. This distinction kept Alzheimer’s in a clinical backwater for decades. If severe memory loss in a 75-year-old was just “getting old,” there was little urgency to study it.
That view began shifting in the 1970s and 1980s as researchers recognized that the plaques and tangles Alzheimer had found in Auguste Deter’s brain were the same ones appearing in older patients diagnosed with senile dementia. The conditions weren’t separate. They were the same disease striking at different ages.
In 1984, a formal set of diagnostic criteria was adopted by a joint working group of the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer’s Disease and Related Disorders Association. The term “probable Alzheimer’s disease” became the standard research diagnosis, and the condition was almost universally accepted in the research community as a distinct illness rather than a consequence of aging.
How Diagnosis Has Changed
For most of its history, Alzheimer’s could only be confirmed after death, by examining brain tissue under a microscope. A living patient could receive a diagnosis of “probable” Alzheimer’s based on symptoms, but certainty required an autopsy. In the 1990s, neuropathologists settled on defining the disease entirely by the burden of plaques and tangles found in post-mortem brain tissue, regardless of what symptoms the person had shown while alive.
That began to change as brain imaging and lab tests improved. Between 2009 and 2011, the National Institute on Aging and the Alzheimer’s Association developed new guidelines that incorporated biomarkers, measurable biological signs detectable in living patients, into the diagnostic process. For the first time, it became possible to identify the disease’s biological footprint before death.
A 2018 research framework went further, defining Alzheimer’s solely by biomarkers. Under this framework, the disease is present when both abnormal amyloid and abnormal tau markers are detected, whether or not the person has symptoms. Abnormal amyloid alone, without tau involvement, isn’t considered Alzheimer’s, though it may represent an early stage.
The most recent revision, published in June 2024, incorporated blood-based biomarkers into the diagnostic criteria for the first time. Earlier testing required either spinal fluid samples or specialized brain imaging. Plasma-based tests are simpler and more accessible, though the 2024 criteria currently recommend diagnostic testing only for people who are already showing symptoms, not for screening asymptomatic individuals outside of research studies.
From Obscure Diagnosis to Public Health Priority
Alzheimer’s spent most of the 20th century as a diagnosis few people outside of neurology had heard of. Public awareness grew slowly through the 1980s and 1990s as advocacy organizations formed and the number of diagnosed cases climbed alongside an aging population. The National Alzheimer’s Project Act established a coordinated federal strategy to accelerate research, improve early diagnosis, and reduce the burden on patients and families. It created an advisory council bringing together public and private stakeholders and an interagency group to coordinate efforts across the federal government, including international collaboration.
Treatment options remained limited for decades. The first medications approved for Alzheimer’s helped manage symptoms but did nothing to slow the disease itself. That changed in 2021 with the FDA’s approval of the first therapy designed to target amyloid plaques directly, followed in January 2023 by the approval of lecanemab, another amyloid-targeting drug granted accelerated approval. These newer treatments represent a fundamentally different approach: rather than managing symptoms, they aim to remove the protein deposits that drive the disease.
So Alzheimer’s disease has been a named medical condition for roughly 120 years, and the biological process behind it has likely affected humans for millennia, though at far lower rates than today. What has changed dramatically is how we understand it, how we detect it, and the realistic possibility, still in its early stages, of treating it at its biological roots.