Stefan Merrill Block’s grandmother forgot her age, her daughter, and Stefan when he was twelve. He wrote about his grandmother’s experience with Alzheimer’s disease (AD) for the New Yorker (3), with a focus on his grandmother’s “cognitive return to birth,” called retrogenesis.

Like Stefan’s grandmother, nearly 50 million people around the world have AD or related dementia (2), and that number is expected to rise to 131.5 million by 2050 (6). Those with the diagnosis and their loved ones know first-hand the symptoms associated with this neurodegenerative disease, including disorientation and loss of memory. What is occurring on the molecular level inside the body is not as clear, but scientists have steadily advanced our biological understanding of the disease since Dr. Alois Alzheimer first described it in 1906 (1)

What we now know about AD is that the neurological symptoms associated with the disease come from damage to neurons: the network of cells in the brain that rapidly transmit electrical signals to guide the body (5). Effective communication among neurons allowed Stefan’s grandmother to laugh at his jokes and kiss him on the forehead.

Neurons remarkably do even more – they are responsible for maintaining themselves by taking in oxygen and sugar transported by the blood. They are excellent at repairing themselves to last an entire lifetime, unlike other more short-lived cells in the body that are rapidly replaced (5).

Neurons work as part of a support system that helps keep the brain healthy and thriving. This team is composed of supportive filaments, called microtubules, that guide nutrients throughout each neuron, and glial cells that protect neurons from physical and chemical damage (5).

AD is marked by the destruction of this healthy brain system. Brain tissue analysis of AD patients shows a buildup of incorrectly folded proteins called amyloid beta plaques, that collect between neurons and disrupt the intricate system of cell communication and function.

The supportive microtubule filaments are sometimes sabotaged by an aggregation of another protein called tau, which collects inside neurons to form neurofibrillary tangles (7). Additionally, brain inflammation can cause glial cells to accumulate and stop clearing out debris, a failure in their role of protecting neurons from harm (4). Issues in the vasculature of the brain, such as hardening of arteries or accumulation of beta amyloids, can prevent the removal of aggregated toxic proteins (4).

These compounding factors wound neurons throughout the brain, and eventually bring on neuronal death. The patient’s brain is slowly being disrupted by proteins clumping where they don’t belong, a phenomenon presented to us as confusion on their face. These biological events contribute to brain atrophy or shrinkage (6), which is what makes the disease so deadly.

Block said he turns to fiction to understand the feelings of late-stage AD, since those experiencing it often cannot communicate. That question might be left to storytellers for now, but the answers of the causes and cure for AD are still aggressively hunted by scientists. Many advancements have been made in the biological understanding of the disease since Dr. Alzheimer’s discovery in the early 20th century, and many more are yet to come. What advancements would you like to see?

  1. Alzheimer’s Association. (2020). Milestones. Retrieved January 04, 2021, from
  1. Alzheimer’s Statistics. (2020). Retrieved January 04, 2021, from
  1. Block, S. (2014, August 20). A Place Beyond Words: The Literature of Alzheimer’s. Retrieved January 04, 2021, from
  1. Kwon, H. S. & Koh, S. (2020). Neuroinflammation in neurodegenerative disorders: The roles of microglia and astrocytes. Translational Neurodegeneration, 9(1). doi:10.1186/s40035-020-00221-2
  1. NIH National Institute on Aging. (2017, May 16). What Happens to the Brain in Alzheimer’s Disease? Retrieved January 04, 2021, from
  1. Sengoku, R. (2019). Aging and Alzheimer’s disease pathology. Neuropathology, 40(1), 22-29. doi:10.1111/neup.12626
  1. Vogel, J. W., Iturria-Medina, Y., Strandberg, O. T., Smith, R., Levitis, E., Evans, A. C., & Hansson, O. (2020). Spread of pathological tau proteins through communicating neurons in human Alzheimer’s disease. Nature Communications, 11(1). doi:10.1038/s41467-020-15701-2