Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that gradually destroys memory and thinking skills, eventually affecting the ability to carry out the simplest tasks. It is caused by complex changes in the brain that occur over decades, leading to the loss of neurons and their connections. The core question about its spread is straightforward: Alzheimer’s disease is not contagious. It cannot be transmitted through normal daily contact, such as coughing, touching, sharing utensils, or spending time with an affected person. Research into how the disease’s underlying pathology can be accidentally transferred has revealed rare medical circumstances, but these findings do not change the fact that AD is not an infectious disease.
The Established Risk Factors for Alzheimer’s
Alzheimer’s is primarily a disease of internal biological processes and environmental interaction. The greatest known factor influencing a person’s risk for developing the condition is increasing age, with most individuals diagnosed after age 65. After 65, the risk for AD roughly doubles every five years.
Genetics also plays a significant role, though most cases are not inherited in a simple manner. The Apolipoprotein E (APOE) gene, specifically the epsilon 4 variant, represents the strongest known genetic risk factor for late-onset AD. Inheriting one copy of APOE epsilon 4 increases risk, and inheriting two copies increases it substantially.
A range of lifestyle and environmental factors further contribute to an individual’s overall risk profile. Conditions that affect cardiovascular health, such as high blood pressure, diabetes, and high cholesterol, are strongly associated with an increased likelihood of developing AD. Maintaining a healthy diet, getting regular physical activity, and pursuing higher levels of education are considered modifiable factors that may help reduce the overall risk of cognitive decline.
Understanding Protein Misfolding and the Prion Hypothesis
The reason scientists investigate the question of transmissibility relates to the specific biological mechanism that drives Alzheimer’s progression. The disease is defined by the accumulation of two distinct types of misfolded proteins in the brain: amyloid-beta, which forms extracellular plaques, and tau, which forms intracellular neurofibrillary tangles. These proteins are believed to act in a “prion-like” manner, which is the scientific concept that underpins the transmissibility theory.
The term “prion-like” describes how these misfolded proteins can induce normal, correctly-folded proteins to adopt the same abnormal structure, a process known as “seeding.” Once a seed is present, it acts as a template, causing the pathology to spread throughout the brain from one neuron to the next, similar to a chain reaction. This self-propagation explains how the disease pathology moves and worsens within the patient’s brain over time, leading to widespread neurodegeneration.
It is important to differentiate between proteins that act like prions and true infectious prion diseases, such as Creutzfeldt-Jakob Disease (CJD). While the pathology of Alzheimer’s spreads internally through a similar templating mechanism, there is no evidence that the amyloid-beta and tau proteins can be transmitted in a contagious way through the air or casual contact. The prion hypothesis focuses on the internal spread of protein misfolding.
Investigating Accidental Medical Transmission
The scientific concern about the remote possibility of transmission arises from specific, historical medical procedures that inadvertently introduced the misfolded protein seeds into a person’s body. These rare cases, termed iatrogenic (medically induced) transmission, have been documented in individuals who received human growth hormone (hGH) extracted from the pituitary glands of cadavers between 1959 and 1985. This practice was discontinued after it was linked to the transmission of CJD.
Studies performed on some of these patients, decades after their treatment, found that they had developed the characteristic amyloid-beta protein pathology associated with Alzheimer’s. Researchers hypothesize that the hGH preparations were contaminated with amyloid-beta seeds from the cadaveric pituitary tissue. These findings demonstrate that the underlying pathology—the protein misfolding—can be transferred under extremely unusual and invasive circumstances.
The medical community now uses synthetic human growth hormone, eliminating this specific risk entirely. While the studies confirm that amyloid seeds are transmissible, they do not suggest that Alzheimer’s disease itself is contagious, nor that it can be passed on during routine medical care or through blood transfusions. The research highlights the need for continued vigilance regarding the sterilization of surgical instruments used in neurosurgery.