Brain vulnerability

The distribution of NMDAR subtypes offers one explanation for regional brain vulnerability to HIV-associated injury. Neonatal brain predominantly expresses... 

Geula C, Wu CK, Saroff D, Lorenzo A, Yuan ML, Yankner BA. Aging renders the brain vulnerable to amyloid f -protein neurotoxicity. Nature Med. 1998 4 827-831. 

APOE-related pathogenic mechanisms are also associated with brain aging and with the neuropathological hallmarks of AD [17, 28], mtDNA damage may also contribute to increase brain vulnerability and neurodegeneration [29, 30],... 

Geula, C., Wu, C. K., Saroff, D., Lorenzo, A., Yuan, M. and Yankner, B. A. Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity. Nature Medicine 4 827-831 1998. 

The nervous system is vulnerable to attack from several directions. Neurons do not divide, and, therefore, death of a neuron always causes a permanent loss of a cell. The brain has a high demand for oxy gen. Lack of oxygen (hypoxia) rapidly causes brain damage. This manifests itself both on neurons and oligodendroglial cells. Anoxic brain damage may result from acute carbon monoxide, cyanide, and hydrogen sulfide poisonings. Carbon monoxide may also be formed in situ in the metabolism of dichloromethylene. 

Endogenous estrogens are known to be active in a number of areas of the brain. There are indications that estrogens may play a role in mood, locomotor activity, pain sensitivity, vulnerability to neurodegenerative diseases and cognition (McEwan, 1999). In humans, the blood brain barrier is not fiilly developed at birth and, for this reason, the central nervous system (CNS) may be more sensitive to phytoestrogens in utero or at birth. As ERs are expressed in the CNS, phytoestrogens may also be active in this area. 

Bromont, C., Marie, C. and Bralet, J. (1989). Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats. Stroke 20, 918-924. 

The spinal cord emerges from the brain stem at the base of the skull and terminates at the second lumbar vertebra. The thoracic spine is most vulnerable to cord compression because of natural kyphosis and because the width of the thoracic spinal canal is the smallest among the vertebrae. Most spinal cord compression is due to adjacent vertebral metastases that compress the spinal cord or from pathologic compression fracture of the vertebra. This results in significant edema and inflammation in the affected area. 

With disruption of this barrier, molecules such as albumin freely enter the brain and ions and water follow. Because the brain lacks a well-developed lymphatic system, clearance of plasma constituents is slow, edema occurs, and intracranial pressure rises. At lower levels of exposure, subtle dysfunction of the blood-brain barrier may contribute to neurobehavioral deficits in children (Bressler and Goldstein 1991 Goldstein 1993). The particular vulnerability of the fetus and infant to the neurotoxicity of lead may be due in part to immaturity of the blood-brain barrier and to the lack of the high-affinity leadbinding protein in astroglia, which is discussed later in this section. Results of measurements of transendothelial electrical resistance across the blood-brain barrier from mice of various ages showed that lead potentiates cytokines-induced increase in ion permeability of the blood-brain barrier (Dyatlov et al. 

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