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"It is a wicked disease that robs its victims of their memories, their ability to think clearly, and ultimately their lives. For centuries, those afflicted by Alzheimer's disease have suffered its debilitating effects while family members sit by, watching their loved ones disappear a little more each day until the person they used to know is gone forever. The disease was first described by German psychologist and neurologist Alois Alzheimer in 1906. One hundred years and a great deal of scientific effort later, much more is known about Alzheimer's, but it still affects millions around the world, and there is no cure in sight. In The End of Memory, award-winning science author Jay Ingram writes a biography of this disease that attacks the brains of patients. He charts the history of the disease from before it was noted by Alois Alzheimer through to the twenty-first century, explains the fascinating science of plaques and tangles, recounts the efforts to understand and combat the disease, and introduces us to the passionate researchers who are working to find a cure. An illuminating biography of "the plague of the twenty-first century" and scientists' efforts to understand and, they hope, prevent it, The End of Memory is a book for those who want to find out the true story behind an affliction that courses through families and wreaks havoc on the lives of millions"--
"For centuries, those afflicted by Alzheimer's disease have suffered its debilitating effects, with family members watching their loved ones disappear a little more each day until the person they used to know is gone forever. It was in 1901 that German psychologist and neurologist Alois Alzheimer began working with Auguste Deter, a 51-year-old woman suffering from dementia. When several years later upon her death he examined her brain under the microscope, he remarked on two unusual features: dark blobs he called "plaques" and the twisted remnants of neurons, or "tangles." In the century since the disease was first described, there has been a great deal of scientific inquiry into its causes, but little progress in its treatment. Jay Ingram believes we are on the threshold of important new leaps in understanding, and in The End of Memory he explains the fascinating science of plaques and tangles, recounts the imperfect history of our efforts to understand and combat the disease, and introduces us to the passionate researchers who are now working to find a cure. In the spirit of Siddhartha Mukherjee's The Emperor of All Maladies, this is a book for those who want to find out the true story behind an affliction that courses through families and wreaks havoc on the lives of millions"--… (meer)
Good introduction to the current theories about causes of the disease and research into potential treatments / cures. Not an exhaustive overview for the lay person a la The Emperors of Maladies (about cancer), but if you have any interest in learning about Alzheimer's Disease I recommend it. A member of my family has been stricken so I was left depressed and frustrated as it seems we are many decades away from any kind of breakthrough. ( )
Very interesting and informative, and written in Jay Ingram's distinctive style--I could imagine his voice as I read the book. Jay has a talent for presenting complex facts in a digestible way.
Editorial Reviews Review "Riveting...with crackerjack storytelling and fast-paced prose, Ingram examines recent research into Alzheimer's...excellent...a must-read" Publishers Weekly "Cogent and informative...upbeat prose, Ingram demonstrates his optimism about the possibility of aging and an agile mind'" Kirkus "In this deft overview, science writer Jay Ingram unravels the complexities of the science past and present" Nature --This text refers to the Paperback edition.
Informatie afkomstig uit de Engelse Algemene Kennis.Bewerk om naar jouw taal over te brengen.
To my father, Ralph Ingram, for demonstrating dignity, patience and love in caring for my mother through her years of dementia
Eerste woorden
Informatie afkomstig uit de Engelse Algemene Kennis.Bewerk om naar jouw taal over te brengen.
I forget exactly what I was looking for when I came across an editorial in the journal 'Neurology' titled, "Mom and Me."
Citaten
Informatie afkomstig uit de Engelse Algemene Kennis.Bewerk om naar jouw taal over te brengen.
Alzheimer's is, after all, "the plague of the twenty-first century."
It was first called "Alzheimer's disease" about a hundred years ago, and while that coinage created a brief flurry of interest at the time, it wasn't until the mid-1970s that it became recognized as a disease, rather than a common companion of old age.
But two are worth examining: one is the assertion that turmeric is responsible for the extremely low rates of Alzheimer's found in India; the other, the incontrovertible evidence that large amounts of sugar in the diet are not good. Today, this evidence is considered so central to the problem of Alzheimer's that some are calling the disease type 3 diabetes.
Hayflick established that embryonic human cells would divide about fifty times, then die. Conversely, cells taken from individuals in their eighties or nineties divided only a handful of times before expiring. If cells were frozen and stored, then thawed and put back into a culture medium, they just picked up where they had left off, counted to their limit and then died. It showed beyond doubt that cells had built-in limits to their lives.
Regardless, the bottom line is that reproduction is more important than longevity in order to preserve a particular species.
What causes cells to go through life with a built-in constraint on their ability to divide? Hayflick had no clue back in the 1960s, when he discovered the limit, but it's now clear that the major players are telomeres, little caps on the ends of our chromosomes that shrink a bit with every cell division. They apparently function to keep our chromosomes intact, something like the aglets on shoelaces, but with each round of DNA replication as cells divide and their chromosomes replicate, a segment of the telomeres is not copied and is therefore lost.
At the same time, the middle ground of maintaining a reasonable weight might at least protect us from some of the diseases that accompany age.¶ A diet high in antioxidants has also been promoted as a way of delaying aging, as the idea of accumulated damage due to oxygen running wild in your tissues has always held a prominent place in theories of aging. However, the experimental results are inconclusive.
Leonard Hayflick has commented that "death by natural causes" is a rare diagnosis these days, and yet, he argues, many deaths are exactly that, the natural causes being the gradual breakdown of the body as a result of aging.
The statistic that stands out above all others is this: since 1840, life expectancy has risen roughly one year in every four. In the twentieth century alone, life expectancy rose by twenty-five years!
In his view, chronic disease was being successfully postponed, but life span was immutable, so what was formerly a slow decline to death made unpleasant by illness became a full life with such a rapid collision with the life span limit that the graph became "rectangularized"—a little like Wile E. Coyote chasing the Road Runner off a cliff, stopping in mid-air with his legs still flailing, then falling like a stone.
Estimates suggest that obesity could reduce life expectancy by anywhere from one-third to three-quarters of a year. But given that life expectancy has been rising by three months every year, this finding suggests nothing much more than a hiccup in the trend. Even so, such an impact is bigger than that of all accidental deaths combined. And further, as the cohort of obese children moves into adulthood, the health complications they suffer could affect life expectancy much more; one estimate suggests a reduction of two to five years. But there's an uncertain area in current research: one recent survey has suggested that people who are overweight (not obese) actually live longer, a mystifying result that has not yet been adequately explained—or accepted.
Even if we experience the healthiest possible aging, our mental abilities, or at least some of them, will inevitably decline. This is something completely separate from the destruction brought on by brain diseases like dementia, and researchers admit it's often difficult to disentangle the mental decline of healthy aging from the early stages of Alzheimer's or any of the other dementias.
the prefrontal cortex (the part of the brain that was the target of the nortorious psychosurgical procedure frontal lobotomy) loses about 5 per cent of its volume every ten years, and that's every ten years after the age of twenty!
One slightly puzzling finding is that the hippocampus (the part of the brain that was destroyed in K.C. and removed in H.M.) seems not to degenerate as quickly as the prefrontal cortex, and some parts of the hippocampus appear to remain virtually intact over time. (Ironically, those parts are among the hardest hit in Alzheimer's.)
The crucial point about the loss of brain volume with time, in the hippocampus and elsewhere, is that it's the result not of dying neurons but of disappearing synapses.
There are eighty-six billion neurons in the adult brain.
The loss of synapses corresponds to loss of communication between neurons. The number of such connection points is almost incalculable to star with (eighty-six billion neurons, each of which might connect to ten thousand other neurons), but the loss is inexorable. And other issues come into play, to be sure: the myelin-coated "white matter" of the brain declines too, compromising the efficiency of communication, but it's the loss of synapses that contributes most to the decline of the aging brain.
The first sign of pathology in Alzheimer's disease is the loss of synapses; the death of neurons comes later. So maintaining the health of synapses and delaying their loss might be one route of delaying, or even preventing, the onset of dementia.
In the spring of 1906, after painstaking staining and preparations, Alzheimer finally looked down the barrel of his microscope at the paper-thin slices of Auguste Deter's brain. And what he saw was devastation on a vast scale. First, the number of neurons (the brain cells) was dramatically reduced from normal. But he was also struck immediately by two more very unusual features. One of them was this: scattered among the remaining nerve cells were numerous dark spots, which he called "plaques." Although their structure varied slightly, they were essentially dark, round deposits. As odd as the plaques were, they were no stranger than the second odd feature he discovered: "tangles"—twisted filaments, aggregates of stuff inside the brain cells, looking in Alzheimer's drawings like locks of matted hair clumped together with bits and pieces of cell detritus. Some scientists had described them as "flame shaped." They were residues, sometimes the only evidence that told him a neuron had been there before.
Following on the conclusive studies of the 1960s that plaques and tangles were indeed the agents most closely associated with Alzheimer's disease, a competition was launched: scientists who believed that the disease process started with amyloid countered those who assigned the key role to tau. At one point in this decades-long debate, people joked that the conflict had become a quasi-religious sparring match between tau believers and amyloid beta believers, Tauists versus BAptists.
If an effective treatment for the disease is to be developed, it has to be targeted toward the agent of the disease. And these days, it's beginning to look as if the ultimate target might be neither plaques nor tangles.
The key idea is that the development of Alzheimer's is a process. There is pretty good evidence that we all start accumulating at least some plaques and tangles much earlier than you might expect, perhaps as early as thirty or forty. It's not inevitable that they reach the levels diagnostic of Alzheimer's disease; it's not even certain that if you do have that many of them in your brain, you are going to be demented. Nonetheless, the fact is that both are the final products of a long chain of production and aggregation. Plaques arise from the dumping of amyloid from neurons; tangles arise from the accumulation of excess and nonfunctional tau inside them. What's not so clear is whether or not these end products actually trigger the damage of the disease.
Idea density is a curious thing: you write an essay when you're twenty-one or twenty-two and then put it away. Take it out many decades later, and it'll tally with your cognitive abilities at that older age.
Advanced education, even getting a Ph.D., didn't seem to moderate the decline in linguistic ability.
This result has been confirmed in other studies as well, with the conclusion that people with dementia often have issues with cerebral blood supply in addition to plaques and tangles.
One factor does clearly accelerate cognitive decline, however: impending death, the phenomenon known as the "terminal drop."
there appears to be a sudden slump in cognitive ability three to four years prior to death.
But one thing is clear: by the time the course of the disease has reached the point of overt destruction of the brain, it has taken up residence in the entorhinal cortex, a small area on each side of the brain, tucked under the massive cerebral cortex.
the important point is that the entorhinal cortex and the hippocampus are intimately related—in anatomy as well as in function. Disrupting the entorhinal cortex would clearly affect memory and then the mental functions dependent on memory, which, frankly, include most of them. One study established that in cognitively intact individuals, the entorhinal cortex houses something like seven million neurons, a number that is stable from the age of sixty to ninety. But as Alzheimer's takes hold, those numbers decline precipitously, in some places in the entorhinal cortex by as much as 90 per cent.
the ability to detect the smell of peanut butter declines perceptibly in the very early stages of Alzheimer's.
This odd inverse relationship has prompted a theory that Alzheimer's is really a disease of evolutionary history. It's well known that the process of wrapping insulation around neurons is complete in chimps long before the process is complete in humans, and it's perhaps notable that non-human primates never get Alzheimer's, no matter how long they live.
In 1988 a team led by Robert Katzman revealed that plaques and tangles were fairly common in the brains of people who never suffered from Alzheimer's disease.
The revelations that a significant fraction of dementias appear to have been prevented due to improvements in cardiovascular care have moved the role of the brain's blood supply back into the spotlight.
Their main points were that aging itself appears to play a more central role in Alzheimer's than does amyloid and that amyloid, while likely a player, is just that: a player, not the centre of the Alzheimer's universe.
Selkoe is a prominent supporter of the dominant scenario, the "amyloid cascade" (the idea that the accumulation of amyloid leads to plaque, tangles, synapse destruction and cell death, eventually overwhelming the brain). But he agrees that plaques might protect in the sense that they mop up the short pre-plaque aggregates and prevent them from causing damage.
This is a reminder of the fact that late-onset Alzheimer's is malleable: diet, exercise, education, a mentally challenging occupation, conscientiousness and likely many more as-yet-unidentified influences play a role in creating the brain reserve that is considered to protect against these genetic effects.
The APOE gene sits on chromosome 19 and exerts its effects in myriad ways. It influences the inflammatory response to infection, it is intimately involved with cholesterol (moving it in and out of cells, not just in the brain but all over the body) and the APOE4 version can cause abnormal brain blood flow and slower recovery from head trauma in teens and young adults (and head trauma is a predisposing factor in Alzheimer's).
The least cognitive decline measured over a six-year period was found in those who ate more than two vegetable portions a day on average. It was a substantive protection too, equivalent to reducing age by five years (remembering that age is the biggest risk, bar none, for Alzheimer's). Green leafy vegetables were the most effective, but the big puzzle was the lack of benefit associated with eating fruit.
In the midst of all this uncertainty, however, one food-related substance is unambiguously associated with Alzheimer's and dementia, and that is sugar.
Type 1 diabetes is the result of the body's immune system mistakenly attacking and destroying insulin-producing beta cells in the pancreas, thus shutting down the production of insulin.
People who have type 2 diabetes have double the risk of getting Alzheimer's.
two new blood tests for Alzheimer's, or at least tests to foresee the development of the disease, were announced: one based on a set of ten fat molecules in the blood, the other on a set of ten proteins. In both cases, the combination of results from all ten could predict progression to Alzheimer's over the next few years with 80 or 90 per cent accuracy.
Laatste woorden
Informatie afkomstig uit de Engelse Algemene Kennis.Bewerk om naar jouw taal over te brengen.
I'd be excited to live long enough to see the whole thing resolved. It will be one day, but that day is not exactly on the horizon.
"It is a wicked disease that robs its victims of their memories, their ability to think clearly, and ultimately their lives. For centuries, those afflicted by Alzheimer's disease have suffered its debilitating effects while family members sit by, watching their loved ones disappear a little more each day until the person they used to know is gone forever. The disease was first described by German psychologist and neurologist Alois Alzheimer in 1906. One hundred years and a great deal of scientific effort later, much more is known about Alzheimer's, but it still affects millions around the world, and there is no cure in sight. In The End of Memory, award-winning science author Jay Ingram writes a biography of this disease that attacks the brains of patients. He charts the history of the disease from before it was noted by Alois Alzheimer through to the twenty-first century, explains the fascinating science of plaques and tangles, recounts the efforts to understand and combat the disease, and introduces us to the passionate researchers who are working to find a cure. An illuminating biography of "the plague of the twenty-first century" and scientists' efforts to understand and, they hope, prevent it, The End of Memory is a book for those who want to find out the true story behind an affliction that courses through families and wreaks havoc on the lives of millions"--
"For centuries, those afflicted by Alzheimer's disease have suffered its debilitating effects, with family members watching their loved ones disappear a little more each day until the person they used to know is gone forever. It was in 1901 that German psychologist and neurologist Alois Alzheimer began working with Auguste Deter, a 51-year-old woman suffering from dementia. When several years later upon her death he examined her brain under the microscope, he remarked on two unusual features: dark blobs he called "plaques" and the twisted remnants of neurons, or "tangles." In the century since the disease was first described, there has been a great deal of scientific inquiry into its causes, but little progress in its treatment. Jay Ingram believes we are on the threshold of important new leaps in understanding, and in The End of Memory he explains the fascinating science of plaques and tangles, recounts the imperfect history of our efforts to understand and combat the disease, and introduces us to the passionate researchers who are now working to find a cure. In the spirit of Siddhartha Mukherjee's The Emperor of All Maladies, this is a book for those who want to find out the true story behind an affliction that courses through families and wreaks havoc on the lives of millions"--
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