@article{oai:hirosakiuhw.repo.nii.ac.jp:00000020,
 author = {吉村, 教暤},
 issue = {1},
 journal = {弘前医療福祉大学紀要},
 month = {Mar},
 note = {Article, AD is a rapidly increasing dementia whose measure for medical and social welfare has been a serious
social problem in Japan. The brain lesions of AD are characterized by 3 main histological changes:
NFT, SP, and loss of neurons. With the reexamination of an AD case with a 25 year-clinical course as
an opportunity, the author revealed the maximal range of occurrence of NFT and SP in AD. The results
showed that neurons were classi›ed into 3 types: neuron types with NFT-rich, NFT-rare, and NFT-free.
As to the pathogenesis of AD brain lesions, it is known that Aβ deposition occurs first and the
oligomers with the highest toxicity develop into proto›brils and ›brils and ›nally form neuritic plaques
which contain degenerated neurites. In addition, Aβ oligomers generated in and around synapses and
inside neurons are considered to induce cell death due to the toxicity to neurons and glial cells. On the
other hand, it is believed that by GSK3β which is activated by the overproduction of Aβ inside
neurons, hyperphosphorylation of tau proceeds and soluble oligomers of tau polymerize to be insoluble
granular aggregates, and then become larger insoluble NFT. It is still unclear where tau oligomers or
granules associate with Aβ oligomers or proto›brils to develop NFT and Aβ ›brils, respectively, and
what mechanisms play roles to develop NFT in “NFT only tauopathies”. Detailed analyses that
reveal all of differences between NFT-rich and NFT-free neurons may open a road to pathogenetic
mechanisms of NFT formation., 弘前医療福祉大学紀要, 2(1), 2011, p.1-14},
 pages = {1--14},
 title = {The occurrence range of proper lesions (neurofibrillary tangles and senile plaques) to Alzheimer’s disease : patho-anatomical study of a familial Alzheimer},
 volume = {2},
 year = {2011}
}