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This practice guideline focuses on the cognitive assessment for mild cognitive impairment in the Guangdong-Hong Kong-Macao Greater Bay Area. To achieve the standardization and normalization of its clinical practice and generate individualized intervention, the National Core Cognitive Center of the Second Affiliated Hospital of Guangzhou Medical University, the Cognitive Disorders Branch of Chinese Geriatic Society, the Dementia Group of Neurology Branch of Guangdong Medical Association and specialists from Hong Kong and Macao developed guidelines based on China's actual conditions and efficiency, economic cost and accuracy. The article addresses the significance, background, and the process of the assessment and follow-up to realize the promotion and dissemination of cognitive assessment.
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Objective To explore the effect of different types of statins combined with donepezil in the treatment of Alzheimer disease(AD).Methods According to the digital table,90 patients with AD were randomly divided into the statins A group(atrovstatin combined with donepezil) 31 cases,statins B group(simvastatin combined with donepezil)27 cases,and donepezil group(only with donepezil) 32 cases.All patients were treated for one year.The blood lipid level (including cholesterol (CH) and low density lipoprotein cholesterol (LDL-C),mini-mental state examination(MMSE),activity of daily living(ADL) and global deterioration scale (GDS) were detected and compared respectively among groups before and after treatment.Results The MMSE,ADL and GDS scores of the donepezil group were (17.00 ± 2.99) points,(60.44 ± 14.57) points,(4.28 ± 1.22) points,respectively,which were worse than those of the statins A group [(19.90 ± 3.07) points,(71.61 ± 18.50) points,(3.39 ± 1.15) points] (t =0.218,P ＜ 0.05,t =2.669,P ＜ 0.01,t =2.562,P ＜ 0.01) and statins B group [(19.88 ± 6.66) points,(71.89 ± 19.61) points,(3.37 ±l.39)points](t=l.959,P ＜0.05,t=2.991,P ＜0.0l,t=2,265,P ＜0.01).Conclusion The combination of donepezil and statins can effectively improve cognitive function and daily living ability in patients with AD,and its effect is superior to single use of donepezil.
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Missense point mutations, duplication and triplication in the alpha-synuclein (alphaSYN) gene have been identified in familial Parkinson's disease (PD). Familial and sporadic PD show common pathological features of alphaSYN pathologies, e.g., Lewy bodies (LBs) and Lewy neurites (LNs), and a loss of dopaminergic neurons in the substantia nigra that leads to motor disturbances. To elucidate the mechanism of alphaSYN pathologies, we generated TgalphaSYN transgenic mice overexpressing human alphaSYN with double mutations in A30P and A53T. Human alphaSYN accumulated widely in neurons, processes and aberrant neuronal inclusion bodies. Sarcosyl-insoluble alphaSYN, as well as phosphorylated, ubiquitinated and nitrated alphaSYN, was accumulated in the brains. Significantly decreased levels of dopamine (DA) were recognized in the striatum. Motor impairment was revealed in a rotarod test. Thus, TgalphaSYN is a useful model for analyzing the pathological cascade from aggregated alphaSYN to motor disturbance, and may be useful for drug trials.
Subject(s)
Brain/metabolism , Motor Activity/physiology , Neurons/metabolism , alpha-Synuclein/genetics , Acetylcholine/metabolism , Animals , Blotting, Western , Brain/pathology , Corpus Striatum/metabolism , Dopamine/metabolism , Humans , Immunohistochemistry , Inclusion Bodies/metabolism , Mice , Mice, Transgenic , Mutation , Neurons/cytology , Phosphorylation , RNA, Messenger/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Rotarod Performance Test , Serotonin/metabolism , UbiquitinationABSTRACT
Abeta amyloidosis and tauopathy are characteristic changes in the brain of Alzheimer's disease. Although much evidence suggests that Abeta deposit is a critical initiation factor, the pathological pathway between Abeta amyloidosis and tau accumulation remains unclear. Tau accumulation was examined in the doubly transgenic mouse (APP-PS) expressing betaAPP(KM670/671NL) (Tg2576) and presenilin-1 L286V (PS-1 L286Vtg). Accelerated and enhanced Abeta amyloid deposits were detected from 8 weeks. Tau accumulation appeared at 4.5 months and markedly increased in dystrophic neurites around Abeta amyloid. Accumulated tau was phosphorylated, conformationally altered, and argyrophilic. Expression of tau and accumulation of sarkosyl-insoluble phosphorylated tau were increased in APP-PS brains compared with those of Tg2576 mice. Straight or twisted tubules mimicking paired helical filament were revealed at electron microscopic level in 16-month-old APP-PS. These findings suggest that mutant presenilin-1 accelerated Abeta-induced tauopathy and further promoted fibril formation of tau.
Subject(s)
Alzheimer Disease/metabolism , Amyloid beta-Protein Precursor/metabolism , Brain/metabolism , Membrane Proteins/metabolism , Mutation/genetics , tau Proteins/metabolism , Alzheimer Disease/genetics , Alzheimer Disease/physiopathology , Amyloid beta-Protein Precursor/genetics , Animals , Brain/pathology , Brain/physiopathology , Disease Models, Animal , Membrane Proteins/genetics , Mice , Mice, Transgenic , Microscopy, Electron, Transmission , Microtubules/metabolism , Microtubules/pathology , Microtubules/ultrastructure , Neurites/metabolism , Neurites/pathology , Neurites/ultrastructure , Neurofibrillary Tangles/genetics , Neurofibrillary Tangles/metabolism , Neurofibrillary Tangles/pathology , Phosphorylation , Plaque, Amyloid/genetics , Plaque, Amyloid/metabolism , Plaque, Amyloid/pathology , Presenilin-1 , Up-Regulation/geneticsABSTRACT
0.05). ②Plasma endothelin in the two groups was remarkably decreased after treatment(P0.05).③ NO in the two groups was significantly increased after treatment(P0.05). Conclusion TFL can reduce blood pressure and improve endothelial cell function.
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Objective To explore the expression of naturally occurring plasma anti-? amyloid (A?) antibody in children and youngsters .Methods According to each 10 years, 28 healthy cases aged from 1~30 years old were diviedd to 3 groups.In the 3 groups,the plasma anti-A? antibody was detacted by immunostained with paraffin sections from Tg2576 mice brain to make a specific tissue amyloid plaque immunoreactivity (TAPIR) and immunoprecipitation analysis. Results The total occurrence rate of anti-A? antibody was 27.8%. There was no significant difference of TAPIR positive rate in each age group. They had the similar immunospecialties to middle-aged and elderly healthy controls. Conclusion Plasma anti-A? antibody can be occured before amyloid deposits and senile plaques in brain.
