I will share what little I know about the disease. It causes memory loss, physical loss, and loss of reasoning and judgment. Through autopsies of the brains of people with Alzheimer's, we see plaque and tangles in their brains rather than neurons. Their brains have shrunk to a much smaller size. It's as though the disease consumes the brain.
There are different explanations for the tangles and plaque. One source blames something called an amyloid protein for AD. Amyloid is one of various complex proteins that occur in a number of diseases. Scientists heatedly disagree as to whether amyloid causes Alzheimer's or is simply a sign of the disease apart from its source. Many proponents of the amyloid-as-cause theory believe that the depositing of beta-amyloid protein kills neurons and thus causes Alzheimer's. Others believe that the accumulation of the protein tau is a defining feature of Alzheimer's. Tau lives in the cell and holds the cellular structure in shape. According to this theory , tau collapses on itself and becomes tangled. Meanwhile, the amyloid protein, which in a healthy brain is usually a clear liquid, gets gooey and forms plaque between cells, interfering with neural communication. The tau tangles and the amyloid plaque cause brain cell death.
The plaque and tangles start in the hippocampus, which is the central brain area that takes short term memory and converts it to long-term memory. By the time an AD sufferer dies, 50% of the hippocampus is destroyed.
You may well ask, if scientists know that amyloid and tau cause problems in the brain, why can't we stop them? The problem is, we're not sure that's what's causing the Alzheimer's. Even the diagnosis of AD is subjective. You go to an Alzheimer's Research Center and have physical, neurological, cognitive functioning and memory tests. In NYC these centers are located at Mt. Sinai, NYU and Columbia hospitals.
Often people worry that they have Alzheimer's if they forget where they put their keys or forget a name attached to a familiar face. But there are benchmarks that are specific to Alzheimer's. In the early stage, the person starts to lose his or her executive functioning (not being able to manage a checkbook; hard time going grocery shopping; can't come up with a plan and implement it to solve problems; Forgets to pay bills; Starts losing ability to communicate ("searching for words"); Forgets appointments and doesn't recall he or she has one; Loses initiative to organize activity; Grooming changes (not so meticulous).
In the middle stage, the person is: Asking the same question over and over; disinhibited (forgetting social niceties and says what they're thinking without interior censor; Reason and judgment severely impaired; Communication losses continue; Very frustrated; May hallucinate and become paranoid; Can remember more long-term memories as opposed to short-term memories.
In the late stage, all language is lost (maybe retains 1-3 words). Can utter sounds and syllables. Loses ability to walk. Incontinent. Can't feed themselves. Needs 24-hour, around-the-clock care.
It is a sobering list, especially disquieting in light of our ignorance about the cause and treatment for the disease, let alone a cure. There are several FDA-approved drugs on the market that treat the symptoms of the disease. Aricept and Excelon keep acetycoline from being destroyed. Acetylcholine is a neurotransmitter found in the central nervous system. It is a chemical that allows neurons to communicate with each other. Acetylcholine's role in learning and memory is unclear but Deutsch in 1970 believed that because most of the acetylcholine in the neocortex originates in the basal forebrain, that cholingeric synapses themselves were the site for memory storage. These drugs also replace the depleted levels of acetylcholine. Rasidine stimulates brain cells to produce more acetylcholine (it inhibits a naturally-occurring anti-acetylcholine chemical). Other drugs are used to enhance the brain's cholingeric system. The drug Namenda acts like glutamate, another neurotransmitter like acetylcholine. These drugs do not reverse disfunctionality, or even arrest progressive deterioration, but they do extend some functionality over a short time.
However, there are discoveries all the time about possible cures and treatments for Alzheimer's. We mustn't give up hope. I mean, it's true that Alzheimer's is a progressive, degenerative and irreversible neurological disease with no cure, but there are hopeful signs on the horizon. There was an article in the 6/10/07 New York Times on the first page of the Business Section, headlined, "Taking on Alzheimer's". Wyeth Laboratories used a vaccine to attack the amyloid plaque in the brain. (It did have mixed results in human testing, but some patients responded very well.) To prevent any more side effects, Wyeth decided against continuing to use a vaccine to induce natural antibodies in the participant. They developed passive immunization, infusing participants with the antibody product bapineuzumab.
At Wyeth's research laboratory, scientists tested this product on mice that had been genetically altered to induce Alzheimer's. Normal mice could remember where a raised platform was in a pool after they found it once, but the genetically altered mice couldn't. They kept swimming around in circles, unable to find dry ground. After they were treated with bapineuzumab, they were able to remember better where the platform was, and in scan pictures their brains improved. They had less plaque and tangles than they did before they were given bapineuzumab.
In a more recent article in the 6/11/07 New York Times, patients in a drug trial treated with the antihistamine Dimebon did better than those receiving a placebo on all five measures of cognition and behavior. As with the other drugs mentioned, Dimebon treats the symptoms, not the underlying disease.
The results of the drug trial after 12 months showed that patients on the drug were better or the same as at the start of the trial. This suggests that the drug improves functionality, not merely slowing decline.
People affected by Alzheimer's disease, whether they are caregivers, persons with Alzheimer's or in the family of someone with Alzheimer's, are organizing and becoming politically active, increasingly advocating for more funds for the disease. As the population ages and more become ill, research on Alzheimer's is more urgent than ever.