Discovery of Alzheimer's DiseaseAlois Alzheimer was a German physician who was born in Bavaria, Southern Germany in 1864. Alzheimer was incredibly gifted in school, excelling in science at a young age. He attended college at Berlin, Aschaffenburg, Tübingen and Wurzburg where he studied medicine and received a medical degree in 1887. He started work at a state asylum in Frankfurt where he became very interested in researching the human brain. He and his colleagues spent the following years studying the pathology of the nervous system. In 1903, in search of a job in which he could combine research with clinical practice, he became the research assistant to Dr. Emil Kraepelin at the Munich Medical School. Soon after taking this position, he created a new laboratory specifically designed for neurological research. In 1906, Alzheimer presented the haunting case of Auguste Deter, shortly after her death, to a meeting of his medical peers. Deter was a patient who had significant memory loss, random suspicions about her family, and other gradually worsening psychological changes that Alzheimer had observed. In her brain autopsy, he saw dramatic shrinkage and abnormal plaque deposits in and around nerve cells. Alzheimer discussed his findings on the brain and symptoms of pre-senile dementia publicly in 1906, but the attendees to this lecture were rather uninterested at the time. In his lecture, Alzheimer identified an 'unusual disease of the cerebral cortex' which affected a woman in her fifties (Auguste Deter). The post-mortem examination showed various abnormalities of the brain. The cerebral cortex was noticeably thinner than normal and senile plaque, which was previously only encountered in elderly people, was found in the brain along with neurofibrillary tangles. Following this lecture, he published a short paper which summarized his lecture; followed by a long paper in 1907 detailing the disease and all of his findings. In 1910, the disease was officially named by his boss and mentor, Dr. Emil Kraepelin, after Dr. Alzheimer. (Alzheimer Disease International) (Hippius, Hanns, and Neundörfer)
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Neurological Information
Alzheimer's Disease is characterized by progressive degenerative neuronal changes and the overall deterioration of the brain's cognitive and personality functions. The disease is believed to begin in the medial temporal lobe structures that are responsible for memory (entorhinal cortex and hippocampus) and then they gradually spread to the surrounding areas of the brain. The disease commences with the accumulation of the beta-amyloid (AB) protein, which leads to the formation and deposition of amyloid plaques throughout the hippocampus. When this occurs, neuronal damage, inflammation, interrupted neuronal communication, and the initiation of neurofibrillary tangle (NFT) synthesis soon follow. As NFTs accumulate, they cause tau proteins (protein surrounding microtubules) in the brain to gradually build up. This causes neurons to become inflamed which produces a reduction in communication, function, and eventually the neurons die. As the cells and neurons from various regions of the brain die, the brain begins to shrink and lose its ability. This process of NFT accumulation begins mainly in the medial temporal lobe. This area of the brain is the region that is responsible mainly for the memory of an individual, both short and long term. It next spreads to the limbic system and the neocortex. The limbic system is what is responsible for your emotions such as anger, depression, fear, happiness, etc. The neocortex is responsible for your speech and hearing ability. Finally, the entire cerebral cortex is affected by the disease. The cerebral cortex is the entire outer layer of the brain which is responsible for the majority of the functions of the brain. (DeFina)
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Progression of Alzheimer's Disease over time and the physical effects of it on the different areas of the brain
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