My own ideas on cause of memory loss
Copyright George Christos 2003
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Current theories of the cause of Alzheimer's disease (AD) do not address the question as to why AD patients initially and gradually lose their short-term memory, followed later by progressive and accelerated loss of other memory, language, motor skills, perception and very short-term memory. We propose that this pattern of memory loss may be a result of a REM sleep deficit or malfunction. This hypothesis is also supported by :
(1) Results which show that AD patients have less REM sleep than controls.
(2) There is an established close correspondence between learning/memory and REM sleep. REM sleep deprivation is known to result in (mild) impairment in learning recent information.
(3) AD patients have a degenerated cholinergic system of the brain. The cholinergic system is known to activate/stimulate the REM sleep process.
(4) The lesions in AD victims are primarily located in those regions of the brain that are considered to be active during REM sleep.
(5) There is a natural mechanism by which the REM sleep in humans is reduced from 8 hours each day at birth to less than one hour each day in old age. An acceleration of this process can lead to possible REM deficit at old age. Furthermore, since old people have so little REM sleep they are more vulnerable to a REM sleep deficit.
The REM sleep deficit mechanism may also work in conjunction with other theories of the etiology of AD, in which case, the REM sleep deficit may explain the progression and/or the acceleration of memory loss in AD. If our ideas are correct, it offers hope that the memory loss in AD may be alleviated or reduced by prolonged periods of increased REM sleep. REM sleep deficit may also be useful for early diagnosis of AD disease. Our hypothesis can be tested by more detailed studies of the amount of REM sleep in patients with AD, particularly in the early stages of the disease.
Here is a link
to some drugs used to treat Alzheimers's disease. Note that the first 3
are cholinesterase inhibitors work by slowing down the process that
breaks down a key neurotransmitter. Donepezil, galantamine and
rivastigmine are cholinesterase inhibitors.