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Biomedical subjects

K Kristensson

Publications and source records attributed to K Kristensson.

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

Potential role of viruses in neurodegeneration.

Viruses have the capacity to induce alterations and degenerations of neurons by different direct and indirect mechanisms. In the review, we have focused on some examples that may provide new avenues for treatment or altering the course of infections, i.e., antibodies to fusogenic virus membrane proteins, drugs that interfere with lipid metabolism, calcium channel blockers, immunoregulatory molecules, and, and inhibitors of excitotoxic amino acids. Owing to their selectivity in attack on regions of nervous tissue, governed by viral factors and by routes of invasion, viral receptors or metabolic machineries of infected cells, certain viral infections show similarities in distribution of their resulting lesions in the nervous system to that of the common human neurodegenerative diseases (namely, motor neurons disease, Parkinson's disease, and Alzheimer's disease). However, it should be emphasized that no infectious agent has as yet provided a complete animal model for any of these diseases, nor has any infectious agent been linked to them from observations on clinical or postmortem materials.

Alzheimer Disease↗
PubMedDate not supplied

Dynamics of Ia-expressing cells and T lymphocytes of different subsets during experimental allergic neuritis in Lewis rats.

Inflammatory cells were characterized by immunohistochemistry, utilizing monoclonal antibodies against cell surface antigens in frozen sections of sciatic nerves and nerve roots of Lewis rats, sacrificed during the course of experimental allergic neuritis. Large numbers of Ia-expressing irregular macrophage-like/dendritic cells, as well as W 3/13 reactive T lymphocytes of both W 3/25 reactive helper and ox8 reactive suppressor/cytotoxic phenotypes were seen within afflicted peripheral nervous tissue at the start of clinical symptoms and at the height of the disease. T lymphocytes of both helper and suppressor/cytotoxic phenotypes decreased concomitant with clinical recovery. During this period demyelination was still extensive and Ia-expressing macrophage-like/dendritic cells were abundant.

Animals↗