One of the proteins belonging to the transmembrane 4 superfamily, T-cell acute lymphoblastic leukemia-associated antigen 1 (TALLA1), behaves like a potential tumor-associated antigen. Furthermore, its mRNA is expressed in normal brain. We examined here the histochemical localization of the protein and its mRNA in human brain tissues. Both nonneurological and Alzheimer disease (AD) brains showed astroglial staining for the TALLA1 molecule. In AD brain tissues, globular dystrophic neurites were positively stained. In damaged white matter showing leukoaraiosis by CT scan there was varicose axonal staining with the anti-TALLA1 antibody. In situ hybridization histochemistry using a RNA probe demonstrated neuronal expression of the mRNA. These results suggest that TALLA1, like amyloid precursor protein or chromogranin A, is produced in neurons and transported by axonal flow.

Aged↗

PubMedDate not supplied

Localization and expression of cdc2 and cdk4 in Alzheimer brain tissue.

Two regulators of the eukaryotic cell cycle, cell division cycle 2 (cdc2) and cyclin-dependent kinase 4 (cdk4), have been reported to be related to Alzheimer's disease (AD) pathology, and especially to hyperphosphorylated tau protein. Using well-characterized polyclonal antibodies which recognize the C termini of cdc2 kinase and cdk4, we examined by immunohistochemistry brain tissues from patients with non-neurological conditions, AD and cerebral infarction. Semiquantitative mRNA analysis by RT-PCR was also done using non-neurological and AD brains. In AD, as previously reported, the antibody to cdc2 showed positive staining of a few intracytoplasmic neurofibrillary tangles (NFTs). In addition, this antibody gave positive immunolabelling in astrocytes and capillaries in all brains studied. In both AD and cerebral infarct cases, the staining of astrocytes was more intense than in non-neurological brain tissue. In all cases, the antibodies to cdk4 showed positive immunolabelling in the nuclei of all cell types except neurons. In AD tissue, the antibody showed additional staining of neuronal nuclei and cytoplasm. In contrast to a previous report, we did not find positive labelling of NFTs with the anti-cdk4 antibody. In infarct areas, particularly strong nuclear staining in glial cells was seen. The relative levels of cdk4 mRNA in AD brains were higher than those in controls. These data suggest that cdc2 kinase appears in glial cells capable of cell division and may play a role in the regulation of amyloid precursor protein processing and NFT formation in neurons. As suggested in a report on rat brain, neuronal expression of cdk4 may reflect some pathological process in damaged cells in AD.

Aged↗

PubMedDate not supplied

Interrelationship between beta-amyloid deposition and complement-activated oligodendroglia.

Complement-activated oligodendroglia (CAOs) are thought to represent complement bearing damaged oligodendroglia for opsonization. The interrelationship between CAOs and amyloid deposits was examined by immunohistochemistry in the parietal lobe of patients with Parkinson's disease, diffuse Lewy body disease, and pallido-nigro-luysial atrophy. In all brains, the anti-C4d antibody stained numerous CAOs. Anti-beta-amyloid protein (anti-A beta) antibody revealed moderate numbers of senile plaques, including some of the classical type. In both the grey and the white matter amyloid deposits were frequently associated with the myelinated axons of CAOs. CAOs were occasionally associated with phagocytosing microglial cells. Immunoelectron microscopy also showed a close relationship between phagocytosing microglia and A beta deposition. On some occasions. A beta deposits were seen in C4d-positive oligodendroglial cell bodies. These results indicate that damaged myelinated axons, which contain accumulated amyloid precursor protein, are the source of A beta, and that CAOs may be initial targets for A beta deposits forming the classical senile plaques.

Adult↗

PubMedDate not supplied

[A case of primary central nervous system lymphoma with the onset of impotence].

A 51-year-old man suffered from impotence for 10 months. Five months before he developed difficulty in urination and walking because of his both leg weakness. He was admitted to the hospital because of urinary incontinence, paraplegia and occipital headache. Neurologic examination revealed neck stiffness and Lhermitte's sign. The cranial nerves were intact with the exception of choked disc. He had weakness of lower extremities and right arm, and sensory loss on the right side including face. The plantar responses were extensor bilaterally. MR images revealed diffuse swelling in the cervical and thoracic spinal cord on a T 1-weighted image without enhancement by Gd-DTPA and diffuse high intensity of the spinal cord on a T 2-weighted image. MR image of the brain revealed the low intensity in the left temporal and occipital lobe with slightly enhancement by Gd-DTPA, the high intensity in the left temporal and occipital lobe white matter on a T 2-weighted image. Diagnosis of malignant lymphoma (B cell type) was made by brain biopsy. Combined chemotherapy was performed and his symptoms resolved and the lesions on MRI disappeared. The number of cases of primary spinal intramedullary malignant lymphoma was very rare and the majority of the cases had weakness or sensory impairment in the lower extremities in the initial symptoms. This is the first case which had impotence as the initial symptom. In addition, it must be taken into consideration of this disease when the patient has myelopathy with unknown etiology.

Brain Neoplasms↗