Alzheimer’s disease is named after Dr. Alois Alzheimer. Alois Alzheimer was a German psychiatrist and neuropathologist in the early 1900s and was the first individual to describe symptoms we now know to be consistent with Alzheimer’s disease. In 1901, Dr. Alzheimer observed a 51-year-old woman named Auguste Deter who presented strange behavioral symptoms including short-term memory loss. Dr. Alzheimer continued to follow Auguste Deter until her death in 1906. Using her brain and medical records, Dr. Alzheimer discovered amyloid plaques and neurofibrillary tangles in Auguste’s brain – these anomalies (amyloid plaques and neurofibrillary tangles) are now the hallmark pathologies associated with Alzheimer’s disease. 

“Dementia” is a general term used to describe a decline in mental ability severe enough to interfere with one’s daily life. Different conditions can cause dementia. Alzheimer’s disease is a specific disease diagnosed by the presence of amyloid plaques and neurofibrillary tau tangles and is the most common cause of dementia.

A number of changes take place in the brain of a person with Alzheimer’s disease. Scientists are still working to understand which changes may cause Alzheimer’s and which are the results of the disease. 

Amyloid plaques are composed of amyloid-beta protein. Amyloid-beta protein is formed from the breakdown of a larger, naturally occurring, protein known as an amyloid precursor protein (APP). The breakdown of APP can generate amyloid-beta proteins of different length – for example, amyloid-beta-42 (or AB42) is an amyloid-beta protein that is 42 amino acids long. Other common forms of amyloid-beta generated during APP breakdown are AB38 and AB40. AB42 is believed to be especially toxic to the Alzheimer’s disease brain. In the Alzheimer’s brain, abnormally high levels of amyloid-beta protein clump together to form plaques – these plaques get wedged between brain cells (neurons) and make it very difficult for them to communicate effectively. Amyloid plaque pathology begins to develop decades before an individual has any disease-associated symptoms. 

Neurofibrillary tangles are abnormal accumulations of tau protein inside neurons (brain cells). In healthy neurons, tau helps stabilize the cell structure. In Alzheimer’s disease, abnormal chemical changes cause tau proteins inside neurons to stick together, forming tangles inside neurons. These tangles block the neuron’s internal transportation system, making it difficult for the neuron to communicate with other neurons.  

The presence of amyloid-beta plaques and tau neurofibrillary tangles leads to chronic inflammation in the brain. Chronic inflammation can further damage neurons.

As these pathologies continue to develop, neurons throughout the brain become injured and die. Over time, this may cause brain regions to shrink (a process called atrophy). 

To date, there is no cure for Alzheimer’s disease, rather current treatment strategies focus on temporarily improving symptoms of the disease (memory loss and problems with thinking and reasoning). Available treatments work to boost the performance of chemicals (sometimes referred to as neurotransmitters) in the brain that carries information from one brain cell (neuron) to another. While these treatments are temporarily beneficial, they do not stop the underlying cause of decline or the death of additional brain cells. As more brain cells die, Alzheimer’s disease continues to progress. Scientists are currently working to develop new disease-modifying treatments for Alzheimer’s disease – these new drug classes include antibodies targeting amyloid plaques, antibodies targeting tau neurofibrillary tangles, and antibodies working to target the immune system. 

Beyond therapeutics, lifestyle modifications such as diet, exercise, proper sleep hygiene, and stress reduction have been shown to help protect the brain against Alzheimer’s disease, in part by maintaining healthy blood pressure. Relevant studies include SPRINT MIND, SPRINT MIND 2.0, WW FINGERS, and US POINTER, among others. 

• Note: we should strive for “normal”, not necessarily low blood pressure, keeping in mind that normal blood pressure is defined by a range of acceptable values. Individuals should consult their doctor to understand their normal values.