Alzheimer's

What is Alzheimer's, and is it different from dementia? In short, yes—Alzheimer's is a specific brain disease that falls under the umbrella of dementia. However it is the most prevalent form of the condition, accounting for 60 to 80% of reported dementia cases.

The brain has three main parts—the cerebrum, brain stem, and cerebellum—each combining to control the entirety of the body’s operations. Alzheimer’s progressively deteriorates the circuitry in these structures, resulting in what we see as the symptoms of the disease.

Brain imaging studies reveal poor sleep leads to production of amyloid beta proteins—molecules linked to Alzheimer’s—which are cleaned from the brain during high-quality sleep. These findings suggest conditions like sleep apnea and insomnia increase the risk of developing the disease.

Dementia villages are specially designed residential communities tailored for individuals with dementia. These environments offer residents a safe, familiar, and stimulating atmosphere resembling normal daily life, promoting greater independence, social interaction, and quality of life, while discreetly integrating necessary care and support from trained professionals.

The first case of Alzheimer's disease dates to the early 20th century when Dr. Alois Alzheimer came across 51-year-old Auguste Deter, struggling with sudden memory issues and aggressive, irrational behavior. After Deter's death, Alzheimer examined her brain and found strange collections of molecular pileups.

Ancient medical texts seldom mention severe cognitive decline, suggesting that such conditions were uncommon. This scarcity is attributed to factors like shorter lifespans and active lifestyles, implying that modern environmental and lifestyle changes—along with longer life expectancy—contribute to the current prevalence of dementia.

Drugs recently approved to slow the progression of Alzheimer's appear to work best when administered as early as possible. Early stages are marked by a low buildup of tau, a protein experts believe clumps into misfolded, neuron-disrupting tangles once clusters of another protein—amyloid beta—have already started causing damage.

The cause of Alzheimer’s disease has been debated for decades. The amyloid cascade hypothesis—where plaques build up in the brain, triggering neurodegeneration—has long been the leading theory. But after a number of failed drug trials, researchers are beginning to reevaluate various culprits.

The complexity of Alzheimer's disease, coupled with decades of underfunded research efforts, has left patients with little in the way of effective treatments. In recent years, scientists have synthesized several drugs that studies show can slow the progression of Alzheimer's—though the disease itself remains incurable.

Neurobiologist Karl Herrup makes the case for reevaluating current research paradigms and embracing a more comprehensive understanding of Alzheimer's disease. He highlights years of failed clinical trials of drugs reducing amyloid plaques in treating Alzheimer's, the establishment of that theory based on a single patient, and more.