With Dr. Alois Alzheimer laying down the groundwork in 1906, the amyloid plaques and neurofibrillary tangles that showed up on his microscope slides from his patients’ brain tissue samples are now identified as the main cause of dementia in individuals with Alzheimer’s disease. Dr. Alzheimer’s findings should have raised a furor and spawned a flurry of research considering that many persons at an advanced age of 65 and above are diagnosed with dementia. The exact opposite happened. When Dr. Alzheimer died in 1915, he seemed to have taken with him the impetus on unlocking the puzzle to Alzheimer’s disease.
It was not until the 1970s that progress was once again made with the cholinergic hypothesis that linked Alzheimer’s disease to the lack of the neurotransmitter acetylcholine in the brain. It spawned the use of cholinesterase inhibitors to improve memory function and reduce the symptoms of Alzheimer’s disease.
With research on the disease once again gaining traction, the 1980s brought more gains to the fight against Alzheimer’s disease. The beta-amyloid protein was identified as a major precursor of the senile plaques seen by Dr. Alois Alzheimer. Cell mutations that enhance excessive production of beta-amyloid proteins, or amyloid cascade, contribute to the accumulation of amyloid plaques. The body’s immune system works against the amyloid plaques by producing an inflammatory response and destruction of brain cells. A working hypothesis was now in place that can identify individuals who are at risk of Alzheimer’s disease.
In 2011, a committee of experts proposed a new model on the progression of Alzheimer’s disease in an individual. It is now thought that an asymptomatic stage precedes the onset of symptoms. During this stage that can last for years, the disease can be caught in its early stage by monitoring amyloid accumulation in the body. A pre-dementia stage soon follows where mild symptoms of dementia are exhibited. In the final stage, full symptoms of dementia are observed in patients. It is the most critical stage for a patient with Alzheimer’s disease. Because there is no treatment available to cure the disease, current medications can only hope to slow down its progression.
by Carl Kegerreis, author of the book, I Wish I Had Those Gasoline Pellets
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