Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The multiple chemical sensitivities syndrome is a symptom complex characterized by emotional depression, short-term memory loss, acquired intolerance to environmental agents such as aerosolized petrochemicals and foods, and alteration in metabolic rate associated with increased body mass. This syndrome can be caused by multiple etiologic agents. With careful evaluation, it is rare that a causal agent can not be identified in this syndrome. Our treatment regimens include combinations of diet and environment control as well as antiviral, antifungal, and immune modulator therapy. We find that the majority of patients can, through time and appropriate treatment, be restored to a normal and productive lives.
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PMID:Multiple chemical sensitivities: a practicing clinician's point of view. Clinical and immunologic research findings. 141 97

Recently, many papers have reported the physiological functions of amyloid beta and amyloid precursor protein (APP). In particular, one of its functions is of importance for synaptic plasticity. Extracellular amyloid beta may suppress synaptic plasticity or inhibit long-term potentiation (LTP) from outside the cell. LTP is now considered the molecular basis of memory. Amyloid beta may induce the inhibition or loss of memory. We propose that suppression of LTP by amyloid beta induces a kind of physiological forgetfulness. On the other hand, homocysteic acid (HA) which is released from astrocytes under stress conditions accumulates the amyloid beta into neuronal cell, which consequently induces the inhibition of amyloid beta physiological function and induces strong LTP. We propose that HA induces strong unforgetful memory under stress condition such as PTSD and emotional depression. The situation is different in the elderly people. Prolonged stress in the elderly people may induce neurodegenerative diseases such as Alzheimer's disease. We observed that in the presence of excess methionine, HA induced alpha-synuclein protein in cultured cells, suggesting a hypermethylation model in vivo. Usually hypermethylation is observed in the ageing process. We have shown that HA promotes the accumulation of amyloid beta in cells, and that the production of alpha-synuclein, which induces the aggregation of amyloid beta, impairing the cell function. LTP is inhibited by deficient cellular function, which means that memories cannot be formed. In fact, there is confusion of memories in the early stages of Alzheimer's disease. Finally, the aggregated alpha-synuclein induces tau pathology, which induces cell death, leading to Alzheimer's pathology. In conclusion, we propose that HA induces Alzheimer's pathology in the elderly people because of prolonged stress.
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PMID:Prolonged stress will induce Alzheimer's disease in elderly people by increased release of homocysteic acid. 1749 46