The repeated intramuscular injections of aqueous emulsions and alcohol-ether extracts of sterile normal rabbit brains in some manner produced pathological changes accompanied by myelin destruction in the brains of 7 of 8 monkeys (Macacus rhesus). Eight, control monkeys remained well. Cultures from the involved brains remained sterile, and no transmissible agent was demonstrated by means of intracerebral inoculations of emulsions of bits of the brains into monkeys, rabbits, guinea pigs, and white mice.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2133246PMC
http://dx.doi.org/10.1084/jem.61.5.689DOI Listing

Publication Analysis

Top Keywords

accompanied myelin
8
myelin destruction
8
brains monkeys
8
encephalomyelitis accompanied
4
destruction experimentally
4
experimentally produced
4
monkeys
4
produced monkeys
4
monkeys repeated
4
repeated intramuscular
4

Similar Publications

Seipin Deficiency Impairs Motor Coordination in Mice by Compromising Spinal Cord Myelination.

Neuromolecular Med

January 2025

Department of Anatomy, School of Basic Medical Sciences, Shanxi Medical University, No 56, Xinjian Nan Road, Taiyuan, 030001, Shanxi, China.

The integrity of the myelin sheath of the spinal cord (SC) is essential for motor coordination. Seipin is an endoplasmic reticulum transmembrane protein highly expressed in adipose tissue and motor neurons in the SC. It was reported Seipin deficiency induced lipid dysregulation and neurobehavioral deficits, but the underlying mechanism, especially in SC, remains to be elucidated.

View Article and Find Full Text PDF

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) caused by pathogenic immunoglobulin G antibodies to myelin oligodendrocyte glycoprotein is a rare demyelinating disease of the central nerve system (CNS). The clinical phenotypes of MOGAD include acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. At present, the mechanism underlying the disease is unknown.

View Article and Find Full Text PDF

Tumor necrosis factor alpha (TNF-α) is a well-known pro-inflammatory cytokine originally recognized for its ability to induce apoptosis and cell death. However, recent research has revealed that TNF-α also plays a crucial role as a mediator of cell survival, influencing a wide range of cellular functions. The signaling of TNF-α is mediated through two distinct receptors, TNFR1 and TNFR2, which trigger various intracellular pathways, including NF-κB, JNK, and caspase signaling cascades.

View Article and Find Full Text PDF

Blue Light Damages Retinal Ganglion Cells Via Endoplasmic Reticulum Stress and Autophagy in Chickens.

Invest Ophthalmol Vis Sci

January 2025

Laboratory of Anatomy of Domestic Animals, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Haidian, Beijing, China.

Purpose: Because chickens have excellent light perception properties, this study focused on investigating whether monochromatic light can cause photodamage in chicken retinal ganglion cells (RGCs).

Methods: Post-hatching day chickens were exposed to four different light-emitting diode light environments for five weeks, respectively, monochromatic blue light (480 nm), green light (560 nm), red light (660 nm), or white light (6000 K). The mechanisms through which monochromatic light influences the structure of the chicken retina were analyzed by detecting the morphological structure of the retina, gene and protein expression levels, and the ultrastructure of the optic nerve.

View Article and Find Full Text PDF

Demyelination-derived lysophosphatidylserine promotes microglial dysfunction and neuropathology in a mouse model of Alzheimer's disease.

Cell Mol Immunol

January 2025

Department of Geriatrics, Gerontology Institute of Anhui Province, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.

Article Synopsis
  • Microglia dysfunction and neuroinflammation are significant contributors to Alzheimer's disease, but their underlying mechanisms are not fully understood.
  • Demyelination in early Alzheimer's leads to increased levels of lysophosphatidylserine (LysoPS) in myelin debris, which activates the GPR34 receptor, promoting neuroinflammation and cognitive decline.
  • Reducing LysoPS or inhibiting GPR34 can enhance microglial function, decrease amyloid-beta (Aβ) accumulation, and improve memory in mouse models, suggesting targeting the LysoPS-GPR34 pathway could be a valuable therapeutic approach for Alzheimer's.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!