Alzheimer’s Disease (AD) is classified as a Non-Communicable Disease (NCD), meaning it cannot be spread from person to person through infectious means like viruses or bacteria. AD is a progressive neurodegenerative disorder that gradually destroys brain cells, leading to memory loss and a significant decline in cognitive function. As the most common cause of dementia, the disease arises from complex biological processes within the body rather than from an external infectious agent.
Defining Non-Communicable Diseases
Non-Communicable Diseases are chronic, long-duration conditions that are not passed from person to person. A defining characteristic is their non-infectious nature, meaning they are not caused by transmissible agents like parasites, viruses, or bacteria. These diseases typically result from a complex combination of genetic, physiological, environmental, and behavioral factors over an extended period. The World Health Organization (WHO) identifies NCDs as the leading cause of death globally, with major examples including cardiovascular diseases, cancers, chronic respiratory diseases, and diabetes. Because Alzheimer’s disease is a chronic condition driven by internal mechanisms and risk factors, not contagion, it fits the definition of an NCD.
The Primary Causes of Alzheimer’s Disease
The etiology that places Alzheimer’s disease firmly within the NCD category is its origin in internal, non-infectious pathology. The greatest single risk factor for developing AD is advanced age, with the chance of diagnosis doubling every five years after the age of 65. This age-related increase points to a degenerative process occurring within the body over time, not a sudden infection.
Genetic factors also play a significant role, particularly the presence of the Apolipoprotein E (APOE) gene’s E4 allele, which is the strongest genetic risk factor for late-onset AD. A small number of early-onset cases are linked to specific mutations in genes like APP, PSEN1, and PSEN2, which almost guarantee the disease’s development.
The core pathology of the disease involves the abnormal buildup of two proteins in the brain: amyloid-beta and tau. Amyloid-beta forms plaques outside the neurons, while misfolded tau protein creates neurofibrillary tangles inside the cells. These protein accumulations, which interfere with normal cell communication, are the result of internal biological malfunctions exacerbated by aging and genetics, not external pathogens.
Lifestyle and environmental factors act as modifiable risk factors that increase the likelihood of developing AD. Conditions like high blood pressure, high cholesterol, and diabetes, which are themselves NCDs, are associated with an increased risk of Alzheimer’s. Poor sleep patterns, a sedentary lifestyle, and a history of traumatic brain injury are also linked to higher risk.
Clarifying Internal Protein Spread
The confusion surrounding Alzheimer’s communicability often arises from scientific findings related to the spread of its misfolded proteins. Researchers describe the progression of amyloid and tau pathology within the brain using the term “prion-like spread.” This refers to the process where an abnormal protein induces a normally folded protein to also misfold, causing the pathology to propagate along connected neural pathways. This internal propagation is a mechanism of disease progression, not a form of external contagion.
While the misfolded proteins share molecular similarities with true prions, there is no epidemiological evidence that Alzheimer’s can be caught from another person. The disease is not transmitted through casual contact, respiratory droplets, or blood transfusions. The disease is initiated by an individual’s genetic and lifestyle factors, and its complex progression remains confined to the brain of the affected individual.