Alzheimer’s disease (AD) is a progressive disorder that slowly destroys memory and thinking skills, eventually affecting the ability to carry out the simplest tasks. As a form of dementia, it represents a profound neurodegenerative process within the brain. Confusion often arises regarding whether it can be “caught” like a cold or flu. This article explores the established scientific classification of AD, the internal biological processes that cause this confusion, and the true factors that determine an individual’s risk.
Alzheimer’s Disease is Classified as Noninfectious
Alzheimer’s disease is formally classified as a noninfectious, neurodegenerative condition, meaning it is not caused by an external pathogen. Noninfectious diseases arise from a combination of genetic, environmental, and lifestyle factors, rather than a transmissible agent like a virus, bacteria, fungus, or parasite. Unlike infectious diseases, which can spread through contact, AD cannot be transmitted from one person to another through casual exposure. The disease develops internally over many years, showing no evidence of being contagious. This established classification places AD alongside conditions like diabetes, heart disease, and most cancers.
Understanding Protein Misfolding and Propagation
The confusion regarding AD’s infectious potential stems from its underlying pathology, which involves misfolded proteins that spread within the brain in a “prion-like” manner. The defining features of AD are the accumulation of amyloid-beta (Aβ) plaques outside neurons and neurofibrillary tangles composed of the protein tau inside neurons. Both Aβ and tau are proteins that have adopted an abnormal, misfolded shape. These misfolded proteins act as “seeds,” inducing nearby normal proteins to also misfold and aggregate. This process, called propagation or seeding, allows the pathology to spread along interconnected neural pathways, progressively worsening cognitive function. While this self-propagating mechanism is similar to how infectious prions cause diseases like Creutzfeldt-Jakob disease, the process in AD is an internal pathology driven by the brain’s own proteins, rather than by an external, infectious agent.
Established Causes and Primary Risk Factors
The initiation and progression of Alzheimer’s disease are driven by a complex interplay of noninfectious factors. The single greatest risk factor is advancing age, with the likelihood of developing the disease doubling approximately every five years after age 65. While age increases risk, AD is not considered a normal part of aging. Genetic risk factors also play a significant role, categorized into risk genes and deterministic genes. The apolipoprotein E (APOE) gene, particularly the APOE-e4 allele, is the strongest known genetic risk factor for late-onset AD. Inheriting one copy of APOE-e4 increases risk, and inheriting two copies increases it substantially. Deterministic genes, such as mutations in the APP, PSEN1, and PSEN2 genes, are rare, accounting for less than one percent of cases, but they directly cause early-onset familial AD. Modifiable lifestyle and vascular factors also contribute to AD risk, suggesting a strong link between brain health and cardiovascular health.
Modifiable Risk Factors
Conditions associated with increased risk include:
- Mid-life hypertension.
- Type 2 diabetes.
- High cholesterol.
- Obesity.
- Physical inactivity.
- Smoking.
- Excessive alcohol consumption.
- Untreated hearing loss.
These established risk factors underscore the noninfectious nature of AD, linking its onset to an individual’s genetic predisposition and lifetime health history.
Clarifying the Risk of Person-to-Person Transmission
Despite the internal nature of the disease, public concern has focused on the theoretical risk of external transmission of the misfolded proteins. Current evidence is clear that AD is not contagious and cannot be transmitted through routine contact, caregiving, sexual contact, or blood transfusions. There is no epidemiological data suggesting that neurodegenerative diseases spread like traditional infections. However, in extremely rare, historical medical contexts, studies suggested a potential for iatrogenic, or medically induced, transfer of amyloid pathology. This was observed in individuals who received human growth hormone extracted from cadaver pituitary glands, a practice phased out decades ago. The contaminated hormone material contained amyloid-beta seeds, which were linked to the development of amyloid pathology in a few recipients. This research reinforced the need for strict sterilization protocols for neurosurgical instruments, but it does not change the fundamental conclusion: Alzheimer’s disease is not an infectious illness that poses a transmission risk in daily life or contemporary medical practice.