Alzheimer’s disease is a progressive neurodegenerative disorder that slowly destroys memory and thinking skills. This condition is the most common cause of dementia and involves the gradual death of brain cells. Recent scientific discussions about the disease’s mechanisms have raised questions regarding its potential transmissibility. This article provides an evidence-based perspective on whether Alzheimer’s disease can be spread from one person to another.
Is Alzheimer’s Contagious?
Alzheimer’s disease is not contagious or transmissible through typical person-to-person contact. It is not possible to contract Alzheimer’s from an affected individual through actions like coughing, touching, or sharing food. The disease is classified as a neurodegenerative disorder, not a communicable one caused by a virus or bacteria. Alzheimer’s is caused by complex biological processes within the brain, and experts emphasize there is no evidence it can be transferred during everyday life or caregiving.
Understanding Non-Infectious Causes
The development of Alzheimer’s disease is attributed to non-infectious factors. Age remains the single greatest risk factor, with the likelihood of developing the condition doubling approximately every five years after age 65. Genetic predisposition also plays a role, such as inheriting the APOE4 allele, which is associated with a higher risk but does not guarantee the disease will develop.
Lifestyle and environmental factors influence risk. Conditions that negatively affect cardiovascular health, including high blood pressure, high cholesterol, and type 2 diabetes, are considered risk factors. A history of traumatic brain injury (TBI) can also increase the risk, particularly in individuals over age 50.
Iatrogenic Transmission and Prion-Like Proteins
Recent scientific discussions about transmissibility stem from extremely rare instances of “iatrogenic transmission,” meaning a condition caused unintentionally by a medical procedure. These cases involve a historical treatment where patients received growth hormone extracted from human cadavers. Some batches of this cadaver-derived human growth hormone (c-hGH) were contaminated with misfolded proteins that caused Creutzfeldt-Jakob disease (CJD). Researchers recently found evidence of amyloid-beta (A\(\beta\)) pathology in the brains of some c-hGH recipients.
The A\(\beta\) and tau proteins central to Alzheimer’s pathology exhibit “prion-like behavior.” This means the misfolded proteins can act as a “seed” to induce normal, healthy proteins to change shape and misfold, leading to aggregation. This seeding mechanism is similar to how true prions spread, but Alzheimer’s is not a classic prion disease. The accidental transfer of these A\(\beta\) seeds in contaminated growth hormone, or possibly through historical medical routes like contaminated neurosurgical instruments, initiated the pathological cascade in certain patients. Modern medical practices use synthetic growth hormone and employ strict sterilization protocols, essentially eliminating this theoretical risk.
How Alzheimer’s Pathology Spreads Internally
The disease’s progression is defined by the accumulation of two distinct abnormal protein structures: amyloid plaques, which form outside the neurons, and tau tangles, which twist inside the neurons. Scientists describe the progression using a seeding or templated mechanism, where the misfolded proteins propagate from one brain region to the next.
The pathology often begins in the lateral entorhinal cortex, a region that serves as a gateway to the hippocampus. From this initial point, the abnormal amyloid and tau proteins travel along the brain’s existing connected neural networks. The toxic proteins move from one brain cell to the next, often using the synapses as a point of transfer. This internal pathological process causes sequential cellular damage and leads to the progressive loss of memory and cognitive functions.