TY - JOUR
T1 - Effect of genetic risk factors and disease progression on the cerebrospinal fluid tau levels in Azheimer's disease
AU - Arai, Hiroyuki
AU - Terajima, Masanori
AU - Miura, Masakazu
AU - Higuchi, Susumu
AU - Muramatsu, Taro
AU - Matsushita, Sachio
AU - Machida, Nobuo
AU - Nakagawa, Takuma
AU - Lee, Virginia M.Y.
AU - Trojanowski, John Q.
AU - Sasaki, Hidetada
PY - 1997/10
Y1 - 1997/10
N2 - OBJECTIVE: This study was undertaken to gain insights into the clinical utility of measuring cerebrospinal fluid tau protein (CSF-tau) to aid in the diagnosis of Alzheimer's disease (AD). SETTING: AD patients from Tohoku University Hospital, Sendai Japan were sampled. SUBJECTS AND METHODS: CSF- tau levels were examined by sandwich enzyme-linked immunosorbent assay in a total of 62 patients carrying different α1-antichymotrypsin (ACT) and presenilin-1 (PS-1) polymorphic alleles. Further, the CSF-tau levels were followed up on two occasions during the progression of the disease in 17 AD patients. RESULTS: There was no evident gradient for tau protein in CSF. Neither the ACT/A allele nor the PS4/1 allele affected the CSF-tau levels. Although CSF-tau levels changed to a variable extent over time, the CSF-tau levels were significantly increased (P < .01) during the follow-up period. Three of the AD patients demonstrated decreasing values, whereas 14 patients showed increasing values. Finally, these temporal changes in CSF-tau levels were not influenced by the apolipoprotein E ε4, ACT/A or PS-1/1 alleles during the progression of AD. CONCLUSION: Regardless of the mechanisms leading to the degeneration of neurons in AD, our findings provide further evidences that monitoring CSF-tau levels may provide useful information about AD irrespective of the background of genetic risks and disease progression.
AB - OBJECTIVE: This study was undertaken to gain insights into the clinical utility of measuring cerebrospinal fluid tau protein (CSF-tau) to aid in the diagnosis of Alzheimer's disease (AD). SETTING: AD patients from Tohoku University Hospital, Sendai Japan were sampled. SUBJECTS AND METHODS: CSF- tau levels were examined by sandwich enzyme-linked immunosorbent assay in a total of 62 patients carrying different α1-antichymotrypsin (ACT) and presenilin-1 (PS-1) polymorphic alleles. Further, the CSF-tau levels were followed up on two occasions during the progression of the disease in 17 AD patients. RESULTS: There was no evident gradient for tau protein in CSF. Neither the ACT/A allele nor the PS4/1 allele affected the CSF-tau levels. Although CSF-tau levels changed to a variable extent over time, the CSF-tau levels were significantly increased (P < .01) during the follow-up period. Three of the AD patients demonstrated decreasing values, whereas 14 patients showed increasing values. Finally, these temporal changes in CSF-tau levels were not influenced by the apolipoprotein E ε4, ACT/A or PS-1/1 alleles during the progression of AD. CONCLUSION: Regardless of the mechanisms leading to the degeneration of neurons in AD, our findings provide further evidences that monitoring CSF-tau levels may provide useful information about AD irrespective of the background of genetic risks and disease progression.
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U2 - 10.1111/j.1532-5415.1997.tb03775.x
DO - 10.1111/j.1532-5415.1997.tb03775.x
M3 - Article
C2 - 9329486
AN - SCOPUS:0030883782
SN - 0002-8614
VL - 45
SP - 1228
EP - 1231
JO - Journal of the American Geriatrics Society
JF - Journal of the American Geriatrics Society
IS - 10
ER -