[科普]健忘与阿兹海默症（英⽂）
其实是我⼀篇病理学作业，那教授着实与众不同，要求⽤通俗易懂的⽂字来写科学review，结果就写成了⼀篇科普⽂，左右写了，故贴上来，有兴趣看的就当增长见闻吧：）
（哪天⼼情好再翻译成中⽂XD）
Why People Become so Forgetful Once They Get Alzheimer's Dia?
Have you ever heard about a dia called Alzheimer's? I bet most of
you probably have heard of it from somewhere, even though you might
not know exactly what it is. For many people who are out of the
science world, "Alzheimer's" means the same thing as "nile
dementia", which is actually incorrect if you speak scientifically.关于爱的名言警句
More interestingly, "dementia" itlf has two different meanings in
the clinical realm and the lay public. "Demented" is generally ud by
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the lay public synonymously with "mad" or "insane". In clinical term
however, dementia refers to a specific and pronounced decline of
cognitive function in humans - a decline in mentation. (In Latin,
dementia means "apart from mind".) "Senile dementia", often shortened
as simply "dementia", refers to the progressive cognitive decline
keepingfound in elderly people beyond what might be expected from normal
aging, which is usually due to damage or dia in the brain. In
specific, dementia can ari from a number of caus such as stroke,
vascular problems, some medical conditions, or the abu of drugs or
alcohol. But among them, a pathological condition called Alzheimer’s
dia (AD) is the most common cau of nile dementia. Becau of
this, it becomes that the two terms, AD and dementia, are often ud
interchangeably in public content. However, plea keep in mind that
there are other caus that can lead to dementia besides AD.
In 1906, a German psychiatrist Alois Alzheimer first described the
dia that eventually bears his name. He wrote of a 51-year-old
woman named Mrs. Auguste D who had "a strange dia of the cerebral
cortex" that manifested as progressive memory impairment and other
behavioral and cognitive problems. After Mrs. Auguste D. died in 1906,
Dr. Alzheimer carefully examined her brain anatomy and neuropathology.
He prented Mrs. Auguste D's ca to the German psychiatrist
community and described the neurofibrillary tangles and amyloid
plaques that were found in Mrs. Auguste D’s brain (Alzheimer,
1907). “Tangles” and “plaques” have then come to be considered as the
two main pathological hallmarks of the dia.
Simply speaking, the plaques are admixtures of a bunch of junks that
brain produces. They are found in the extracellular spaces, i.e. the
outside of the brain cells. A typical nile plaque usually contains
lots of aggregated proteins called amyloid beta (Ab). Scientists have
no idea why our brain produces such protein since it appears to have
no function roles. As this junk protein aggregating into a toxic den
core, the nearby dendrites and axons (the extensions of neurons) are
affected and start dying. In contrast to extracellular plaques, the
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cond pathological hallmark of AD is localized intracellulary, i.e.
inside of the cells. Many people may have an impression that a cell is
like a small squishy water balloon (at least I ud to think so),
which of cour is not true. The cell actually has its own skeleton
structure inside that supports its external shape. It is called
microtubule cytoskeleton. In AD, the microtubules and mircofibrils
become tangling up with each other for some reason. And eventually the
tangles cau the collap of the cytoskeleton, which leads to the
cell death. Remember how your kitten can make a ball of wool into a
fearful tangle? Same thing can happen in our brain, but we haven’t yet
found that "naughty kitten" which caus the neurofibrillary tangles.
Plea don't think tangles and plaques are unique in Alzheimer's. Your
brain is also producing plaques as you reading this line. Tangles and
plaques can be found in many normal non-demented elderly, but rather
in a very reduced number and would not cau vere neuronal loss and
dramatic cognitive problems. One major task for AD rearchers is to
find out why the plaque and tangle forming process are much more
accelerated and pronounced in AD.
Now you are probably wondering how the pathological alterations at
the cell level can lead to the behavioral and cognitive changes in AD patients. Among the symptoms of dementia caud by AD are loss of learning and memory capacity, decline in reasoning ability, attention problems, language difficulties and problems with perception. Forgetfulness is the most typical prenting symptom showed by AD patients in the beginning stage. The patients can reme
mber how to talk, and may remember events from many years ago, but they have trouble remembering what happened in the past hours. Episodic memory formation is lost as the patients typically lost the recollection of
their ongoing experiences on a daily basis. Common examples of memory deficits in this stage are the repetition of questions or statements
and the misplacement of items. The patients at this early stage of AD
are unable to recall recent conversations or events, whereas the past
life experience and knowledge learned years ago are still retrievable, clearly showing the impairment in new information acquisition but not
in the retention of old memory.
The early symptoms of AD remind the scientists of the cognitive changes manifested by another group of patients who lost their hippocampus. Hippocampus (meaning “ahor” in Greek) is a structure located in the medial temporal lobe of our brain. It got its name from
its curved shape in coronal ctions of the brain, which much
rembles a ahor. Today, the hippocampus is generally believed to play a crucial role in the formation of new declarative memories about experienced events. A fancy scientific term of this process is
called “memory consolidation”. In brief, the hippocampus rves as a short-term memory store that eventually uploads memory to the neocortex for longer-term storage. I know many people like to draw an analogy between human brain and computer (indeed, in Chine language, the word “computer” literally means “electronic brain”). If you look
the brain as a super powerful computer, the hippocampus will be its
RAM (random access memory) which temporarily stores information and later uploads them to the hard disk, i.e. the neocortex, for permanent storage. What if the function of the hippocampus is disrupted? Let’s
look at the famous ca of a patient named H.M. H.M. is an unfortunate victim of neurosurgical experimentation who had his medial temporal lobes removed as a treatment for epilepsy, the removed parts including most of his hippocami on both sides of his brain. The lesion partially treated the epilepsy but esntially completely destroyed H.M.’s
capacity of forming long-term memory. He became unable to form any new long-lasting declarative memories (anterograde amnesia) and has been living a minute-to-minute existence for the past five decades of
years. However, his prior memories are mostly intact for his lifetime
螳螂捕蝉up to veral years before the surgery and he is able to consistently
recall them (Scoville & Milner, 2000).
Surprisingly, most AD patients in the initial stages have shown the
same memory problems experienced by H.M. You then might be thinking, oh, maybe there’s something wrong with their hippocampus! And that’s exactly what the scientists have found out. Early in the cour of AD, plaques and tangles are found particularly abundant in a brain region called “entorhinal cortex” which sits right next to the hippocampus.
This region is like a gateway to the hippocampus, and all the information going into or going out from the hippocampus have to pass through it. Without the input from the entorhinal cortex, the hippocampus cannot function properly. Very soon, the hippocampus职场性骚扰
itlf gets occupied by the plaques and tangles, thus los its
ability to establish or consolidate memory for ongoing events. As the dia progress, the plaques and tangles also start to spread out
to other brain structures, meanwhile the initially affected areas are worning. In brief, the circuitry that is critical for normal
declarative memory, i.e. the hippocampus and its adjacent region
appear to be the first target affected by AD neuropathology such as plaques and tangles. That is why people start to become so forgetful
once they get Alzheimer's dia.
The sadness is that the “forgetfulness” is only a start for AD
patients. As the plaques and tangles start to spread out to other
limbic regions and cerebral cortices, patients in the middle stage
have even more profound anterograde memory loss and also start to show retrograde amnesia. That is, recalling remote memories of long past
life experience and events becomes difficult now. Recognition of known
individuals progressively declines and verbal communication becomes incoherent. In many cas, AD patients also display mood disorders such as vere depression, since the victims are aware that they are deteriorating mentally and are “losing” loved ones. Eventually in the final stages of AD, during when the whole neocortex as well as other brain structures are profoundly affected by tangles and plaques, the patients become unable to execute the most basic cognitive functions, thus are unable to take care of themlves. They are completely bedridden until death.
In the days, AD affects up to half million of people in Canada (Canadian Study of Health and Aging Working Group, 2000), 4 million in US, and 12 million worldwide over the age of 65. It is estimated that
by the year 2025 the number will go up to 20 million worldwide given the fact that at prent there is no effective treatment for this dia. The dry statistical numbers probably don’t mean much to you at first glance. Let's look at it in this way then. Right now, about
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one in ten people over the age of 65 in North America have AD. If you live to age 85, you have about a one in two chance of developing this tragically debilitating dia. To me the statistics are sobering, especially given that we don’t have any effective treatment for AD. Since last century, human longevity has been greatly incread worldwide due to our expanding knowledge in biology and great improvement of health care and public hygiene. In the 18th century,
the average human lifespan was around 30 years. But in the year 2005, the average life expectancy in Canada was estimated to be 80.1 years. Some scientists predicted that the USA would have 5.3 million people aged over 100 in 2100. Yes, thanks to the great Science. Nowadays we human are able to treat lots of dia and actively change our living environment to accomplish our longevity dream. But, today’s scientific advances are only able to make our bodies live longer, not our brains. It appears that our brain has a shorter “lifespan” than our bodies.
Our brain starts to gradually degenerate irreversibly as early as incad圆形阵列
our 20's. In addition to the “normal aging”, we are facing more aggressive neurodegenerative conditions such as Alzheimer's that we haven't yet found a weapon to fight against. Does it make n to become a centenarian while losing the ability to recognize your loved ones and losing all th
e precious memory from your past life? I don't know yours but my answer is a big NO. We need a healthy and functioning brain to make our longevity meaningful. While scientists worldwide are working so hard to ek treatments for Alzheimer’s and other brain dias, plea remember that your brain, just like the
rest of your body, need to be looked after. It is your own responsibility to take care of your own precious brain.
K.Fan
Reference:
Alzheimer A. (1907) Uber eine eigenartige Erkrankung der Hirnrinde. Allgemeine Zeitschrift fur Psychiatrie und Psychisch-gerichtliche Medizin. 64:146-48.
Canadian Study of Health and Aging Working Group: Canadian Study of Health and Aging Working Group. (2000) The Incidence of Dementia in Canada. Neurology. 55: 66-73.
Scoville WB, Milner B. (2000) Loss of recent memory after bilateral hippocampal lesions. 1957. J. Neuropsyychiatry Clin. Neuroscie. 12:103-13.
