Fighting the Good Fight Against Alzheimer’s Disease

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

How Alzheimer’s Disease Gained Notoriety

Auguste Deter was loud and disoriented. It took a lot of effort from the Frankfurt Psychiatric Hospital staff and the clinical psychologist, Dr. Aloise Alzheimer, to contain her. Showing signs of paranoia because of sleep disturbance and marked memory lapses, Frau Deter came across as a very intriguing patient to Dr. Alzheimer that fateful day in 1901. When the patient admitted in confusion that she had lost herself in response to a probing question, Dr. Alzheimer knew that it could be a breakthrough case.  

Past forward to 1906. Dr. Alzheimer was informed that after unsuccessfully battling her lingering illness, his patient Frau Deter had succumbed to its ravages. His former head at the hospital, Dr. Emil Sioli, was kind enough to send Dr. Alzheimer samples of her brain material for his further study knowing that he had closely followed the case. With his background in neuroanatomy, Dr. Alzheimer examined the brain tissues under a microscope and paved the way for the identification of what is now known as Alzheimer’s disease- a collection of messy neurofibrillary tangles and clusters and large deposits of amyloid plaques. Afflicting mostly people over the age of 65, the brain shrinks over time as the disease progresses and causes dementia. Looking at the samples, Dr. Alzheimer did not wonder anymore why Frau Deter exhibited strange and recalcitrant behavior.  

Dr. Aloise Alzheimer formally presented his findings on Auguste Deter’s malady to a conference of South-West German Psychiatrists on November 3, 1906. He expected a grilling from his peers in the profession because of the gravity of the findings. Instead, there were very few questions raised. It was a case of the politics of the profession getting in the way of a sublime moment in medical history. In 1909, Dr. Alzheimer republished his findings along with that of other patients who exhibited the same bewildering condition as that of Frau Deter. In 1910, the eminent German psychiatrist, Emil Kraepelin, a friend of Dr. Alzheimer, included a narration of Frau Deter’s case in his psychiatry textbook. It was Dr. Kraepelin who named the illness, Alzheimer’s disease in honor of the work done by his colleague.

by Carl Kegerreis, author of the book,  I Wish I Had Those Gasoline Pellets

Finding a Cure in the Dark for Alzheimer’s Disease

There is no known cure for Alzheimer’s disease. The disease that is upending the lives of an estimated 6.2 million Americans over the age of 65 is free to continue its grim march onward. More than a century has passed since it was first brought into the consciousness of the scientific community by Dr. Aloise Alzheimer, yet, research scientists are still at a loss as to the exact mechanism of its attack on the brain cells. The human body, in all its complexities, still finds a way to elude discovery of its inner workings.

Dr. Alzheimer’s research in 1906 on senile plaques and neurofibrillary tangles forming in brain cells opened the world’s eyes to the stark reality of Alzheimer’s disease and the insidiousness of dementia that it inflicts on hapless patients. With the brain’s neurons progressively destroyed because of the plaques and tangles, the brain shrinks affecting memory. Because ideas are limited on why there is an accumulation of beta-amyloid plaques and the formation of tau protein tangles inside the brain, formulation of a decent cure has been next to impossible. 

With no cure in sight, medical professionals have resorted to medication to stem the onslaught of Alzheimer’s disease. Most of these intercessory treatment drugs are centered on the prevention and limitation of senile plaque accumulation and neurofibrillary tangle formation. One of those popularly used is the cholinesterase inhibitors. They work by inhibiting the cholinesterase enzymes from breaking down acetylcholine, the body’s main neurotransmitter and essential to memory function. Cholinesterase inhibitors help alleviate symptoms of Alzheimer’s disease such as depression, agitation, and aggressiveness. Donepezil, galantamine, and rivastigmine are some of the most-prescribed cholinesterase inhibitors.

Memantine is another drug that is used to contain Alzheimer’s disease. It is used to regulate the concentration of glutamate, another important neurotransmitter that affects learning and memory. It has proven to be effective in alleviating symptoms of moderate to severe Alzheimer’s disease and is sometimes taken in combination with donepezil. 

Aducanumab is the latest drug approved by the Food and Drug Administration for the treatment of Alzheimer’s disease. It is directed toward the removal of amyloid plaques in the brain.

by Carl Kegerreis, author of the book,  I Wish I Had Those Gasoline Pellets

What Alzheimer’s Disease Mean to You and Me

Why should we care about Alzheimer’s disease? The term is as foreign to us as the Greek alphabet or the Mayan calendar. For the estimated 6.2 million Americans aged 65 and older who currently live with the disease according to a report made by the Alzheimer Association, finding the cure to the disease is an urgent race against time. The figures are increasing every minute. By 2050, 12.7 million Americans aged 65 and over will have suffered from the dreaded Alzheimer’s dementia. 

Alzheimer’s disease is a progressively degenerating disease that wreaks havoc on the brain cells or neurons.  The development of beta-amyloid protein plaques outside the brain’s neurons and the tangles of tau proteins inside the neurons lead to the destruction of the brain cells and the brain to shrink. The damage done to the brain manifests as dementia in patients with Alzheimer’s disease. Memory loss, language, and problem-solving difficulties, and continuous decline in thinking skills that affect an individual’s daily activities are the main indicators of dementia. 

The exact cause of Alzheimer’s disease is still a matter of debate. That the neurons die and lose connection to each other is well-accepted. However, the sequence of destructive events inside the brain cells that lead to their death has not been fully explained. Scientists and medical professionals all agree that several risk factors contribute to the probability of developing Alzheimer’s disease. The major risk factors are:

- Age. People who are 65 and over are most at risk of developing Alzheimer’s disease

- Genetic. Those who harbor a certain apolipoprotein E gene type known as APOE-e4 are most susceptible to beta-amyloid accumulation. 

- Family history. Someone who has a parent or sibling with Alzheimer’s disease has a bigger probability of developing the disease.

- Down Syndrome. People with Down syndrome are also likely to fall prey to the disease due to the presence of three copies of chromosome 21 (trisomy 21) in their genes.

- Traumatic brain injury. The likelihood of Alzheimer’s disease in individuals with head trauma increases with the number of traumatic brain injuries sustained.

by Carl Kegerreis, author of the book,  I Wish I Had Those Gasoline Pellets