We have reported abnormality of distribution, composition and phosphorylation level of neurofilament proteins in Alzheimer brains. The protein amounts of neurofilament L (NF-L) and H (NF-H) in Alzheimer and control brains were measured by western blotting to investigate the pathologic changes of neurofilament proteins in Alzheimer brains in detail.Frozen blocks of frontal lobe were homogenized with 2 volumes (v/w) of 10 M urea, and centrifuged at 100,000 x g. The supernatants were analyzed by western blotting using four monoclonal antibodies bound to NF-H (NE-14, SMI-34, SMI-32, N52) and a polyclonal antibody (anti-TL) bound to tail region of NF-L. The protein amounts recognized by the antibodies were densito-metrically analyzed by Image Master (Pharmacia). The standard curves were prepared by the data of experiments of purified NF-H and NF-L, and the protein amounts recognized by the antibodies were calculated.NE14 and SMI-34 bound to phosphorylated epitope of NF-H showed that NF-H content of Alzheimer brains was approximately 1 μg/mg protein, which was almost identical to that of control brains. SMI-32 bound to non-phosphorylated epitope of NF-H showed that NF-H content of Alzheimer brains was approximately 60 % of that of control brains (0.74 μg/mg protein). N52 phosphorylation-independently bound to NF-H showed NF-H content of Alzheimer brains was approximately 1.7 μg/mg protein, which was almost identical to that of control brains. These results indicate the decrease of non-phosphorylated form of NF-H in Alzheimer brains despite of constant amount of NF-H. On the other hand, anti-TL bound to NF-L showed that NF-L content of Alzheimer brains was approximately 60 % of that of control brains (4.23 μg/mg protein), indicating the decrease of NF-L in Alzheimer brains.These findings showed abnormal composition of neurofilament subunit proteins and the significant decrease of total NF-L compared with total NF-H in Alzheimer brains. The decrease of non-phosphorylated form of NF-H imply acceleration of phosphorylation or reduction of de-phosphorylation in Alzheimer brains. These abnormalities of neurofilament may induce the disorder of axonal transport, resulting the deterioration of neuronal functions.