Type 2 diabetes mellitus and Alzheimer's disease are both associated with increasing age,and each increases the risk of development of the other.Epidemiological,clinical,biochemical and imaging studies have shown ...Type 2 diabetes mellitus and Alzheimer's disease are both associated with increasing age,and each increases the risk of development of the other.Epidemiological,clinical,biochemical and imaging studies have shown that elevated glucose levels and diabetes are associated with cognitive dysfunction,the most prevalent cause of which is Alzheimer's disease.Cross sectional studies have clearly shown such an association,whereas longitudinal studies are equivocal,reflecting the many complex ways in which the two interact.Despite the dichotomy,common risk and etiological factors(obesity,dyslipidemia,insulin resistance,and sedentary habits) are recognized;correction of these by lifestyle changes and pharmacological agents can be expected to prevent or retard the progression of both diseases.Common pathogenic factors in both conditions span a broad sweep including chronic hyperglycemia per se,hyperinsulinemia,insulin resistance,acute hypoglycemic episodes,especially in the elderly,microvascular disease,fibrillar deposits(in brain in Alzheimer's disease and in pancreas in type 2 diabetes),altered insulin processing,inflammation,obesity,dyslipidemia,altered levels of insulin like growth factor and occurrence of variant forms of the protein butyrylcholinesterase.Of interest not only do lifestyle measures have a protective effect against the development of cognitive impairment due to Alzheimer's disease,but so do some of the pharmacological agents used in the treatment of diabetes such as insulin(especially when delivered intranasally),metformin,peroxisome proliferator-activated receptors γ agonists,glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors.Diabetes must be recognized as a risk for development of Alzheimer's disease;clinicians must ensure preventive care be given to control and postpone both conditions,and to identify cognitive impairment early to manage it appropriately.展开更多
Objective. To research the relations between low- density lipoprotein receptor- related protein gene (LRP) polymorphism, butyrylcholinesterase gene (BchE) polymorphism and Alzheimer’s disease (AD) in Chinese. Methods...Objective. To research the relations between low- density lipoprotein receptor- related protein gene (LRP) polymorphism, butyrylcholinesterase gene (BchE) polymorphism and Alzheimer’s disease (AD) in Chinese. Methods. The gene polymorphisms of LRP and BchE were genotyped in 38 AD cases and 40 controls with polymerase chain reaction- restriction fragment length polymorphism (PCR- RFLP) methods. AD groups were classified according to the LRP C/C genotype and compared with matched controls. Results. AD group had higher frequencies of C/C homozygote (81.6％ vs 60.0％ , P< 0.05) and of C allele (89.5％ vs 76.3％ , P< 0.05),with no significant difference between any of these LRP genotypes classified AD groups and their respective control groups. Conclusions. A positive correlation was found between LRP gene polymorphism and AD, but not between BchE gene polymorphism and AD in Chinese AD cases.展开更多
The acute effects of commercial formulation of chlorpyrifos-ethyl （Dursban ） and the secondary treated industrial/urban effluent （STIUE） exposure on acetylcholinesterase （ACHE） and butyrylcholinesterase （BuChE...The acute effects of commercial formulation of chlorpyrifos-ethyl （Dursban ） and the secondary treated industrial/urban effluent （STIUE） exposure on acetylcholinesterase （ACHE） and butyrylcholinesterase （BuChE） activities in hepatopancreas and gills of Mediterranean crab Carcinus maenas were investigated. After 2 d of exposure to chlorpyriphos-ethyl, the AChE activity was inhibited in both organs at concentrations of 3.12 and 7.82 μg/L, whereas the BuCHE was inhibited only at higher concentration 7.82 μg/L of commercial preparation Dursban~. The exposure of crabs to Dursban （3.12 μg/L） showed a significant decrement of ACHE activity at 24 and 48 h, whereas the BuChE was inhibited only after 24 h and no inhibition for both enzymes was observed after 72 h. Moreover, a significant repression of AChE activity was observed in both organs of C. maenas exposed to 5% of STIUE. Our experiments indicated that the measurement of AChE activity in gills and hepatopancreas of C. maenas would be useful biomarker of organophosphorous （OP） and of neurotoxic effects of STIUE in Tunisia.展开更多
文摘Type 2 diabetes mellitus and Alzheimer's disease are both associated with increasing age,and each increases the risk of development of the other.Epidemiological,clinical,biochemical and imaging studies have shown that elevated glucose levels and diabetes are associated with cognitive dysfunction,the most prevalent cause of which is Alzheimer's disease.Cross sectional studies have clearly shown such an association,whereas longitudinal studies are equivocal,reflecting the many complex ways in which the two interact.Despite the dichotomy,common risk and etiological factors(obesity,dyslipidemia,insulin resistance,and sedentary habits) are recognized;correction of these by lifestyle changes and pharmacological agents can be expected to prevent or retard the progression of both diseases.Common pathogenic factors in both conditions span a broad sweep including chronic hyperglycemia per se,hyperinsulinemia,insulin resistance,acute hypoglycemic episodes,especially in the elderly,microvascular disease,fibrillar deposits(in brain in Alzheimer's disease and in pancreas in type 2 diabetes),altered insulin processing,inflammation,obesity,dyslipidemia,altered levels of insulin like growth factor and occurrence of variant forms of the protein butyrylcholinesterase.Of interest not only do lifestyle measures have a protective effect against the development of cognitive impairment due to Alzheimer's disease,but so do some of the pharmacological agents used in the treatment of diabetes such as insulin(especially when delivered intranasally),metformin,peroxisome proliferator-activated receptors γ agonists,glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors.Diabetes must be recognized as a risk for development of Alzheimer's disease;clinicians must ensure preventive care be given to control and postpone both conditions,and to identify cognitive impairment early to manage it appropriately.
文摘Objective. To research the relations between low- density lipoprotein receptor- related protein gene (LRP) polymorphism, butyrylcholinesterase gene (BchE) polymorphism and Alzheimer’s disease (AD) in Chinese. Methods. The gene polymorphisms of LRP and BchE were genotyped in 38 AD cases and 40 controls with polymerase chain reaction- restriction fragment length polymorphism (PCR- RFLP) methods. AD groups were classified according to the LRP C/C genotype and compared with matched controls. Results. AD group had higher frequencies of C/C homozygote (81.6％ vs 60.0％ , P< 0.05) and of C allele (89.5％ vs 76.3％ , P< 0.05),with no significant difference between any of these LRP genotypes classified AD groups and their respective control groups. Conclusions. A positive correlation was found between LRP gene polymorphism and AD, but not between BchE gene polymorphism and AD in Chinese AD cases.
基金supported by the fund from the Ministry of Scientific Research and Technology, Tunisia (Research Unit of Biochemical and Environmental Toxicology, UR04AGR05)
文摘The acute effects of commercial formulation of chlorpyrifos-ethyl （Dursban ） and the secondary treated industrial/urban effluent （STIUE） exposure on acetylcholinesterase （ACHE） and butyrylcholinesterase （BuChE） activities in hepatopancreas and gills of Mediterranean crab Carcinus maenas were investigated. After 2 d of exposure to chlorpyriphos-ethyl, the AChE activity was inhibited in both organs at concentrations of 3.12 and 7.82 μg/L, whereas the BuCHE was inhibited only at higher concentration 7.82 μg/L of commercial preparation Dursban~. The exposure of crabs to Dursban （3.12 μg/L） showed a significant decrement of ACHE activity at 24 and 48 h, whereas the BuChE was inhibited only after 24 h and no inhibition for both enzymes was observed after 72 h. Moreover, a significant repression of AChE activity was observed in both organs of C. maenas exposed to 5% of STIUE. Our experiments indicated that the measurement of AChE activity in gills and hepatopancreas of C. maenas would be useful biomarker of organophosphorous （OP） and of neurotoxic effects of STIUE in Tunisia.
