KA MA'I O ALZHEIMER: E PREDISPOSE I KA AXONAL NEUROFIBRILLARY DEGENERATION KA NEURON PLASTICITY?
New England Journal of Medicine, Vol. 313, aoao 388-389, 1985
KA MA'I O ALZHEIMER: E HOʻOMAʻI ANA ʻO NEURON PLASTICITY I KA AXONAL NEUROFIBRILLARY DEGENERATION?
I ka Lunahooponopono: Manaʻo ʻo Gajdusek ʻo ka hoʻopau ʻana i nā neurofilaments ke kumu o nā maʻi dementing (Malaki 14 pukana). 1 No ka weheweheʻana i ke kumu o ka hopena o kekahi mau neurons i loko o ka lolo aʻaʻole i nā mea'ē aʻe,'ōleloʻo ia i nā pūnaewele me nā kumu lāʻau axonal nui, no ko lākou koi nui no ka laweʻana i ke axonal, ua pilikia loa i ka pōʻino axoskeletal. He nani ka kuhiakau o Gajduseks akā ʻAʻole hiki ke helu no ka ʻike ʻana i ka liʻiliʻi o nā neurons otor nui i ka maʻi o Alzheimer.
Manaʻo mākou ʻo ka plastic plastic a me ka nui o ka lāʻau axonal hiki ke hoʻokau i nā koi i ka halihali axonal. Ua pili ka plasticity o nā cell neural i nā ʻano kumu trophic,2 ʻO kekahi o ia mau mea e pili ana i ka halihali axonal. ʻO kahi hiʻohiʻona kūpono ka ulu ʻana i ʻike ʻia ma nā terminal septal norepinephrine,3 i hele pū ʻia me ka nui o nā neurofilaments hou.
ʻO nā neurons e hōʻike ana i kahi kiʻekiʻe o ka plasticity e hana paha i ka substrate o ka hoʻomanaʻo a me ke aʻo ʻana; ua pilikia lāua ʻelua i ka maʻi o Alzheimer. Ua pili nā ala norepinephrine me ke aʻo ʻana e pili ana i ka uku, 4 a ua luku ʻia nā cell norephinephrine o ka locus ceruleus i kekahi mau hihia o ʻO ka maʻi o Alzheimer.5 Hoʻopōʻino pū ka Alzheimer degeneration i ka wahi o ke kumu o nā pūnaewele serotonin i loko o ka midbrain raphe, 6 a ua manaʻo ʻia ke serotonin ma ke ʻano he mea uʻi o ka conditioning maʻamau. o latchkey ma ka hoʻomanaʻo paʻakikī ka mālama ʻana a me ka hoʻihoʻi ʻana, 8.9 a e like me ka mea i ʻike nui ʻia, pili ka maʻi Alzheimer me ka nalowale o kēia mau kino cell a me kā lākou enzymes.10 Ma ka cortical level Alzheimer-type deterioration preferentially pā neuron ma associative wahi, most strikingly the hippocampus and amygdala, 11 ʻelua hana nui i ka hoʻomanaʻo.12 Eia kekahi, koho koho ʻia ka degeneration neurofibrillary i loko o nā neurons me nā axons e hoʻopili ana i ka hippocampus me ka cortex entorhinal.13 No ka mea ʻo nā neurons mai kēlā me kēia pūʻulu e hana i nā pilina e pili ana i ka hoʻopili ʻana o ka ʻike,14 e koi ai i kahi kiʻekiʻe kiʻekiʻe o ka plasticity, kākoʻo ko lākou hōʻino ʻana i ka manaʻo e pili ana nā cell e hōʻike ana i ka plasticity nui i ka neurofibrillary disruption.
ʻO ka hoʻohaunaele ʻana i ka mīkini axonal-transport lohi i nā neurons me kahi kiʻekiʻe o ka plasticity hiki ke alakaʻi i ka dysfunction hoʻomanaʻo pervasive, ka hōʻailona kumu o dementia me ka nānā ʻole i ke kumu. Hiki i kēia axonal-filament dysfunction ke hāʻawi i kahi kumu micropathological no ka loulou i kau mua ʻia ma waena o kahi microtubular diathesis a me Alzheimer-type. dementia 15,16 a hoʻopaʻa pū i kahi papa haʻahaʻa o nā maʻi dementing.
J. Wesson Ashford, MD, Ph.D.
Lissy Jarvik, MD, Ph.D.
UCLA Neuropsychiatric Institute
Los Angeles, CA 90024