Science of aging knowledge environment : SAGE KE
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Sci Aging Knowledge Environ · Mar 2006
ReviewSmall-fiber neuropathy: answering the burning questions.
Small-fiber neuropathy is a peripheral nerve disease that most commonly presents in middle-aged and older people, who develop burning pain in their feet. Although it can be caused by disorders of metabolism such as diabetes, chronic infections (such as with human immunodeficiency virus), genetic abnormalities, toxicity from various drugs, and autoimmune diseases, the cause often remains a mystery because standard electrophysiologic tests for nerve injury do not detect small-fiber function. ⋯ Infrequently, the underlying cause of small-fiber dysfunction is identified and disease-modifying therapy can be instituted. More commonly, the treatments for small-fiber neuropathy involve symptomatic treatment of neuropathic pain.
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Peripheral nerve damage results in loss of sensation in the affected region of the body. Oaklander and Brown now report that, in the rat, transection of a peripheral nerve in only one side of the body also results in profound loss of the innervation of the same region on the opposite side of the body. Peripheral nerve damage may also produce persistent (neuropathic) pain conditions that are presumed to arise from maladaptive reorganization of the central nervous system. Thus, the possibility that comparable bilateral changes occur in patients and that such changes contribute to neuropathic pain conditions must be considered.
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Sci Aging Knowledge Environ · Jul 2002
ReviewInnate immunity, local inflammation, and degenerative disease.
The brain lesions associated with Alzheimer's disease (AD), which are referred to as neurofibrillary tangles and senile plaques, are characterized by the presence of a broad spectrum of inflammatory mediators. Surprisingly, these mediators, which include complement proteins, inflammatory cytokines, prostaglandins, and acute phase reactants such as C-reactive protein and amyloid P, are produced by resident brain cells, including neurons. Although secondary to the fundamental pathology caused by the presence of tangles and plaques, there is strong evidence that inflammation exacerbates the neuronal loss. ⋯ Locally produced inflammatory mediators have also been identified in atherosclerotic plaques, along with evidence of complement self-attack. As was previously shown for heart attacks, epidemiological evidence indicates that extended use of nonsteroidal anti-inflammatory drugs (NSAIDs) results in a reduced risk of AD. NSAIDs inhibit the production of prostaglandin inflammatory mediators, but powerful new therapeutic agents might be developed by targeting more critical inflammatory mechanisms, especially the complement system.