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What Causes Alzheimer’s Disease?

It is thought that a variety of factors are involved in the development of Alzheimer’s disease and how it progresses. For the majority of people, there is no one known definitive cause of Alzheimer’s disease; there are various risk factors that may influence the development and course. In many instances, it is thought to be a combination of genetic, lifestyle, and environmental factors.1

Age

Older age is the main risk factor for developing Alzheimer’s disease, and it is thought that age-related changes in the brain can negatively affect nerve cells, leading to damage that may cause Alzheimer’s disease.1 This can include shrinking of certain areas of the brain, inflammation of brain matter, production of free radicals which harm brain cells, and cell breakdown.1 Neurons get damaged, communication pathways between cells are impaired, and brain cells eventually die.

Genetics

Both types of Alzheimer’s – late-onset (diagnosed in mid-60s) and early-onset (diagnosed between one’s 30s and 60s) – have a genetic component to them.1 The majority of diagnoses are late-onset Alzheimer’s disease. While there is not one specific gene that is the single cause of late-onset Alzheimer’s disease, having one of three forms of the APOE gene on chromosome 19: APOE2, APOE3 or APOE4. If you have two copies of APOE4, your risk of getting Alzheimer’s disease increases about 10 times. can increase your risk of developing Alzheimer’s.1 That being said, having this form of the APOE gene does not necessarily mean you definitely will develop the disease; it is merely a risk factor.

People with early-onset Alzheimer’s disease develop symptoms in their 40s and 50s. Some individuals with early-onset Alzheimer’s disease have a type called early-onset familiar Alzheimer’s disease (FAD).1 This is often caused by an inherited change in one of three genes. Less than 1% of Alzheimer’s disease is caused by mutations in these genes. These genes are 1) APP which makes a protein called amyloid precursor protein, 2) PSEN1, which encodes for a protein called Presenilin 1 and 3) PSEN2, which encodes for a protein called Presenilin 2.

All of the mutations also are involved in the cleavage of APP into smaller fragments and are part of a larger process of the development of amyloid plaques in the brain, a hallmark of Alzheimer’s disease.

Lifestyle and environmental factors

There are associations between the development of Alzheimer’s disease and conditions like heart attack, stroke, high blood pressure, diabetes, and obesity. Metabolic syndrome, characterized by high blood pressure, excess body fat around the waist, high cholesterol, and high blood sugar, has been found to be associated with the development of Alzheimer’s disease and cognitive decline.2 More research needs to be done, but lifestyle and environmental factors are potential causes and risk factors that can be modified. Talk with your doctor about your cardiovascular health and metabolic health, and what you can do to minimize your risk of disease. Things like a healthy diet, regular exercise, and keeping your blood pressure, blood sugars, and cholesterol in check can all help keep your body and mind healthy and reduce your risk of Alzheimer’s disease.

While there is no known definite cause of Alzheimer’s disease, research is being done to narrow down possible pathways of causation. Knowing risk factors and how all possible causes may work together to cause disease can help providers and patients work to stay as healthy as possible. If you’re worried about genetic components to Alzheimer’s disease, talk with your doctor about your genetic risk, and whether genetic testing would be beneficial.

Written by: Jaime Rochelle Herndon | Last reviewed: June 2019
  1. National Institute on Aging. What Causes Alzheimer’s Disease? 2017. https://www.nia.nih.gov/health/what-causes-alzheimers-disease Accessed April 3, 2019.
  2. Reitz C & Mayeux R. Alzheimer disease: Epidemiology, diagnostic criteria, risk factors, and biomarkers. Biochem Pharmacol. 2014; 88(4): 640-651. doi: 10.1016/j.bcp.2013.12.024 Accessed April 3, 2019.