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Amyloid β protein levels in cerebrospinal fluid are elevated in early‐onset Alzheimer's disease
Author(s) -
Nakamura Tamiko,
Shoji Mikio,
Harigaya Yasuo,
Watanabe Mitsunori,
Hosoda Kenji,
Cheung Tobun T.,
Shaffer Lillian M.,
Golde Todd E.,
Younkin Linda H.,
Younkin Steven G.,
Hirai Shunsaku
Publication year - 1994
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410360616
Subject(s) - cerebrospinal fluid , alzheimer's disease , medicine , amyloid precursor protein , amyloid (mycology) , disease , degenerative disease , age of onset , pathology , pathophysiology , amyloid β , endocrinology
The 4‐kd amyloid β prrotein (Aβ) deposited as amyloid in Alzheimer's disease (AD) is produced and released by normal proteolytic processing of the amyloid β protein precursor (βAPP) and is readily detected in cerebrospinal fluid (CSF). Here, we present the levels of Aβ in CSF from a total of 95 subjects, including 38 patients with AD, 14 with early‐onset AD and 24 with late‐onset AD, 25 normal control subjects, and 32 patients with other neurological diseases. The level of Aβ decreased with normal aging, and there was a significant elevation in the level of Aβ in the CSF of early‐onset AD patients (4.14 ±1.37 pmol/ml, p < 0.01). Neither Mini‐Mental State nor Functional Assessment Staging were correlated with the amount of Aβ in the CSF. The Aβ/secreted form of βAPP ration was elevated, but the level of α;1‐antichymotrypsin in the CSF did not correlate with the level of CSF Aβ in early‐onset AD patients. Thus, the level of Aβ in the CSF is elevated in early‐onset AD patients and is suggested to be correlated with the pathology in the brain that characterizes AD.