Biomedical subjects

B Wolozin

Publications and source records attributed to B Wolozin.

40 records · Page 3Linked to original sources

PubMed1988

Reexpression of a developmentally regulated antigen in Down syndrome and Alzheimer disease.

ALZ-50 is a monoclonal antibody that recognizes a protein of apparent molecular mass 68 kilodaltons (A68). The protein is present in the brains of patients with Alzheimer disease but is not detectable in normal adult brain tissue. We now report that ALZ-50-reactive neurons are found in normal fetal and neonatal human brain and in brain tissue from neonatal individuals with Down syndrome. Reactive neurons decrease sharply in number after age 2 and reappear in older individuals with Down syndrome and in patients with Alzheimer disease.

Adult↗

PubMed1987

Alzheimer-related neuronal protein A68: specificity and distribution.

We previously reported that the monoclonal antibody Alz-50 recognizes a protein (A68) with an apparent molecular weight of 68,000 daltons in the brains of patients who died with Alzheimer's disease, but not in brain tissue from individuals free of neurological disease. We now report that substantial quantities of this protein are found in brain tissue only from patients with Alzheimer's disease. Although trace amounts of A68 may be detected in cases of Guam-Parkinson dementia complex and Pick's disease, accumulation of A68 in neuronal perikarya and particularly in neuronal processes appears to be a unique feature of Alzheimer's disease. A68 can readily be detected in cerebrospinal fluid after concentration and partial purification. These data, combined with the quantitation of immunoreactivity in other neurological diseases, suggest the usefulness of detection of A68 in cerebrospinal fluid for diagnosis of Alzheimer's disease.

Aged↗

PubMedDate not supplied

Protein alterations in olfactory neuroblasts from Alzheimer donors.

Definitive diagnosis of Alzheimer's disease (AD) is made by pathologic examination of postmortem brain tissue in conjunction with a clinical history of dementia. To date, there are no good biological markers for a positive diagnosis of AD in the living patient. In an effort to identify biological markers useful both in the clinical and pathologic diagnosis of AD, we have investigated disease-specific protein alterations in cultured olfactory neurons. Olfactory neurons are readily accessible by biopsy, can be propagated in primary cell culture as olfactory neuroblasts (ONs), and exhibit several elements of AD brain pathophysiology making them powerful tools for the study of AD. Two-dimensional gel analysis of ON proteins from neuropsychologically evaluated AD donors revealed a set of five proteins (Mr 17-50 kD, pI 4.8-6.7) that were significantly altered in concentration when compared to cells from age-matched controls. Further characterization and microsequence analysis could lead to the identification of proteins that may have important diagnostic or therapeutic value in the treatment of AD.

Aged↗

PubMedDate not supplied

Regulation of apoptosis by presenilin 1.

Familial Alzheimer's disease is transmitted as an autosomal dominant disorder and, in 5-10% of the cases, is caused by mutations in the coding regions of two homologous genes, Presenilin 1 and 2 (PS1 and PS2). Previously, we have shown that PS2, a homolog of PS1. regulates apoptosis induced in neurons by trophic withdrawal or Abeta, and in T-cells by Fas ligand. We now report that PS1 also regulates apoptosis. Both wild-type and the H115Y mutant form of PS1 enhance Fas-mediated apoptosis in Jurkat cells. We also observed that wild-type and the H115Y mutant form of PS1 differentially regulate Jun Kinase, an important enzyme regulating apoptosis.

Aging↗