Alois Alzheimer, a German psychiatrist and neuropathologist, holds a significant place in the history of neuroscience. Born in 1864, his work profoundly influenced the understanding of neurodegenerative diseases, shaping the field of brain research.
Early Life and Medical Career
Alois Alzheimer was born on June 14, 1864, in Marktbreit-am-Main, Bavaria, where his father worked as a notary. He demonstrated an aptitude for science during his schooling in Aschaffenburg, leading him to pursue medical studies at the Universities of Berlin, Tübingen, and Würzburg. He earned his medical degree in 1887; his doctoral thesis focused on ceruminal glands.
In December 1888, Alzheimer began as a resident at the Hospital for the Mentally Ill and Epileptics in Frankfurt am Main, a position he held for seven years. He was later promoted to senior physician. During his time in Frankfurt, he collaborated with Franz Nissl, a leading histopathologist who developed a new method for staining nerve cell bodies, influencing Alzheimer’s interest in neuropathology. This period allowed him to delve into research on the human brain cortex, establishing an archive of autopsy cases that would prove useful throughout his career. In 1903, he moved to Munich to work with Emil Kraepelin, a prominent psychiatrist, where he became the head of the Munich Institute of Psychiatry laboratory.
The Discovery of Auguste D.
A key moment in Alois Alzheimer’s career involved his patient, Auguste Deter. In November 1901, Alzheimer admitted the 51-year-old woman to the Frankfurt asylum. Auguste Deter presented with unusual symptoms, including severe memory loss, disorientation, and hallucinations, which were not typical for someone her age. She also experienced personality changes, paranoia, and periods of shouting.
Alzheimer observed Auguste Deter’s declining condition, noting her symptoms defied conventional medical explanations. Her health deteriorated rapidly, marked by physical decline. Auguste Deter passed away on April 8, 1906, at age 55. Following her death, Alzheimer requested her brain and medical records be sent to him in Munich for a post-mortem examination. This decision allowed him to examine the brain tissue for underlying physical changes.
Understanding the Brain’s Changes
Upon receiving Auguste Deter’s brain, Alois Alzheimer conducted a post-mortem examination, which revealed microscopic abnormalities. He used staining techniques, such as the Bielschowsky stain, to visualize brain tissue. His observations uncovered two types of protein deposits: extracellular amyloid plaques and intracellular neurofibrillary tangles.
Amyloid plaques appeared as insoluble protein aggregates located outside brain cells. Neurofibrillary tangles were tangled nerve fibers found within the neurons. Alzheimer characterized these formations as the defining hallmarks of the disease he had encountered. He noted that the cerebral cortex was also thinner than normal. These findings were important as they provided a physical correlation between observed neurological symptoms and specific changes in brain anatomy, a connection not previously established for this type of dementia.
His Enduring Contribution
Alois Alzheimer’s discovery of brain changes in Auguste Deter laid the groundwork for research into neurodegenerative diseases. His findings demonstrated that dementia was not simply a natural consequence of aging, but a distinct neurological disorder with identifiable biological markers. This insight shifted the scientific perspective on cognitive decline.
His colleague, Emil Kraepelin, named Alzheimer’s disease in his honor in 1910, including it in the eighth edition of his “Handbook of Psychiatry.” Alzheimer continued to contribute to the field, teaching and conducting research. He also co-founded the “Journal for the Entire Field of Neurology and Psychiatry” in 1909. The identification of amyloid plaques and neurofibrillary tangles remains central to the diagnosis and study of Alzheimer’s disease today, forming the basis for ongoing efforts to understand, diagnose, and develop treatments for this condition.