Back in November 2008, I returned to Hong Kong with Julie visiting her mom.
We met her in her home and my God, she has changed so much. She is much thinner than she was couple of years ago. What disturbed us most is she cannot recognized us her daughter Julie and myself. She is unable to take care of herself in her daily routine such as bathing, change clothes not to mention making food for herself. The change is brought about by Alzheimer's Disease.
What then is Alzheirmer's Disease? I check out from the internet and summarized it for boomers' information.
Alzheimer's disease is a brain disorder named after a German physician Dr. Alois Alzheimer. He is the first described this brain disorder back in 1906. Since then, reeearch scientists have learned a lot more about Alzheimer's disease.
Alzheimer's disease begins very subtly and slowly. . People with this condition may have trouble remembering things that happened recently or the names of people they know. Symptoms get worse slowly. People may not recognize family members. Some may have trouble expressing themselves. Simple daily tasks such as speaking, reading or writing all become difficult. Eventually the AD patients may forget daily hygiene such as brushing teeth and combing hai. They don't to take bathe and they don't know how to change clothes. Some may become anxious or aggressive. When they are out of their home they would get astray. Abruptly, they need total care.
Three major competing hypotheses exist to explain the cause of the disease. The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective. Other cholinergic effects have also been proposed, for example, initiation of large-scale aggregation of amyloid,[50] leading to generalised neuroinflammation.
In 1991, the amyloid hypothesis postulates that amyloid beta (Aβ) deposits are the fundamental cause of the disease. It is a compelling theory because the gene for the amyloid beta precursor (APP) is located on chromosome 21, and people with trisomy 21 (Down Syndrome) who thus have an extra gene copy almost universally exhibit AD by 40 years of age. Also APOE4, the major genetic risk factor for AD, leads to excess amyloid buildup in the brain before AD symptoms arise. Thus, Aβ deposition precedes clinical AD. Further evidence comes from the finding that transgenic mice that express a mutant form of the human APP gene develop fibrillar amyloid plaques and Alzheimer's-like brain pathology. An experimental vaccine was found to clear the amyloid plaques in early human trials, but it did not have any significant effect on dementia.
Deposition of amyloid plaques does not correlate well with neuron loss. This observation supports the tau hypothesis, the idea that tau protein abnormalities initiate the disease cascade. In this model, hyperphosphorylated tau begins to pair with other threads of tau. Eventually, they form neurofibrillary tangles inside nerve cell bodies. When this occurs, the microtubules disintegrate, collapsing the neuron's transport system.[61] This may result first in malfunctions in biochemical communication between neurons and later in the death of the cells
We met her in her home and my God, she has changed so much. She is much thinner than she was couple of years ago. What disturbed us most is she cannot recognized us her daughter Julie and myself. She is unable to take care of herself in her daily routine such as bathing, change clothes not to mention making food for herself. The change is brought about by Alzheimer's Disease.
What then is Alzheirmer's Disease? I check out from the internet and summarized it for boomers' information.
Alzheimer's disease is a brain disorder named after a German physician Dr. Alois Alzheimer. He is the first described this brain disorder back in 1906. Since then, reeearch scientists have learned a lot more about Alzheimer's disease.
Alzheimer's disease begins very subtly and slowly. . People with this condition may have trouble remembering things that happened recently or the names of people they know. Symptoms get worse slowly. People may not recognize family members. Some may have trouble expressing themselves. Simple daily tasks such as speaking, reading or writing all become difficult. Eventually the AD patients may forget daily hygiene such as brushing teeth and combing hai. They don't to take bathe and they don't know how to change clothes. Some may become anxious or aggressive. When they are out of their home they would get astray. Abruptly, they need total care.
Alzheimer's - Generic Disease
Causes (abstract from Wikipedia)View more presentations from M. Sibilla.
Three major competing hypotheses exist to explain the cause of the disease. The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective. Other cholinergic effects have also been proposed, for example, initiation of large-scale aggregation of amyloid,[50] leading to generalised neuroinflammation.
In 1991, the amyloid hypothesis postulates that amyloid beta (Aβ) deposits are the fundamental cause of the disease. It is a compelling theory because the gene for the amyloid beta precursor (APP) is located on chromosome 21, and people with trisomy 21 (Down Syndrome) who thus have an extra gene copy almost universally exhibit AD by 40 years of age. Also APOE4, the major genetic risk factor for AD, leads to excess amyloid buildup in the brain before AD symptoms arise. Thus, Aβ deposition precedes clinical AD. Further evidence comes from the finding that transgenic mice that express a mutant form of the human APP gene develop fibrillar amyloid plaques and Alzheimer's-like brain pathology. An experimental vaccine was found to clear the amyloid plaques in early human trials, but it did not have any significant effect on dementia.
Deposition of amyloid plaques does not correlate well with neuron loss. This observation supports the tau hypothesis, the idea that tau protein abnormalities initiate the disease cascade. In this model, hyperphosphorylated tau begins to pair with other threads of tau. Eventually, they form neurofibrillary tangles inside nerve cell bodies. When this occurs, the microtubules disintegrate, collapsing the neuron's transport system.[61] This may result first in malfunctions in biochemical communication between neurons and later in the death of the cells
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