Neuroprotective Effect of Resveratrol via Activation of Sirt1 Signaling in a Rat Model of Combined Diabetes and Alzheimer's Disease.

Background: Alzheimer's disease (AD) and diabetes mellitus (DM) often coexist in patients because having one of these conditions increases risk for the other. These two diseases share several pathophysiological mechanisms, such as specific inflammatory signaling pathways, oxidative stress, and cell apoptosis. It is still unclear exactly which mechanisms associated with DM are responsible for increased AD risk.

Clinical Profiles and Short-Term Outcomes of Acute Disseminated Encephalomyelitis in Adult Chinese Patients.

Background And Purpose: Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disorder that predominantly affects children. Previous studies have mostly involved children in Western developed countries.

Methods: This study retrospectively reviewed the clinical profiles of ADEM in adult Chinese patients.

Effects of resveratrol on apoptosis in a rat model of vascular dementia.

Resveratrol is a natural polyphenol widely present in plants, particularly in the skin of red grapes and in wine. It possesses a wide range of biological effects and exhibits neuroprotective effects in numerous diseases. However, data evaluating the effects of resveratrol in vascular dementia (VaD) are lacking.

Traditional Chinese medicine: a promising candidate for the treatment of Alzheimer's disease.

Alzheimer's disease (AD) is an age-related neurodegenerative disorder, characterized clinically by insidious onset of memory and cognition impairment, emergence of psychiatric symptoms and behavioral disorder, and impairment of activities of daily living (ADL). Traditional Chinese medicine (TCM) is practiced in the Chinese health care system for more than 2,000 years. In recent years, scientists have isolated many novel compounds from herbs, some of which improve dementia with fewer side effects than conventional drugs and are regarded as potential anti-AD drugs.

[Effect of estrogen-depletion and 17beta-estradiol replacement therapy upon rat hippocampus beta-amyloid generation].

Objective: To observe the effects of estrogen depletion and 17beta-estradiol replacement therapy upon ratbeta-amyloid (Abeta) generation and the possible related mechanisms.

Methods: Rat ovaries were ectomized to mimic estrogen-depletion models and then 17beta-estradiol was administered by powdering hormone into soy-free chow as a way of replacement therapy. ELISA was carried out to detect rat hippocampus Abeta levels and alpha- and beta-secretase activities were measured after the experiment.

Involvement of protein trafficking in deprenyl-induced alpha-secretase activity regulation in PC12 cells.

Deprenyl is a selective B-type monoamine oxidase inhibitor and a neuroprotective agent that has been used to slow the progress of Alzheimer's disease for many years. We previously demonstrated that deprenyl could stem amyloid precursor protein processing (APP) toward the non-amyloidogenic pathway through mitogen activated protein kinase (MAPK) and protein kinase C (PKC)-dependent signaling pathways [Yang, H.Q.

Economic impact of dementia in developing countries: an evaluation of Alzheimer-type dementia in Shanghai, China.

The main objective of this study was to assess the economic cost of Alzheimer's disease (AD) in Shanghai, China, as a pilot study for future evaluations. Sixty-seven patients with AD were interviewed, and the information of the AD-related cost and resources used was collected from October 2005 to September 2006. By retrospective analysis, annual costs were calculated and expressed in Chinese renminbi (RMB).

PMS777, a new cholinesterase inhibitor with anti-platelet activated factor activity, regulates amyloid precursor protein processing in vitro.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by progressive impairment of memory and cognition. Previous data have shown that beta-amyloid (Abeta) cascade plays a central role in AD pathophysiology and thus drugs regulate amyloid precursor protein (APP) metabolism may have therapeutic potential. Here the effects of PMS777, a new cholinesterase inhibitor with anti-platelet activated factor activity, on APP processing were investigated.

Protective effects of erythropoietin on tau phosphorylation induced by beta-amyloid.

Neuropathological studies have demonstrated that the presence of neurofibrillary tangles (NFTs) is one of the most prominent pathologic characteristics of Alzheimer's disease (AD). The microtubule-associated protein tau is the major component of NFTs, and its abnormal hyperphosphorylation leads to the destabilization of microtubules, impaired axonal transport, and eventual death of the neurons. The hematopoietic cytokine erythropoietin (Epo) is now considered as a viable agent with regard to central nervous system injury in a variety of cellular systems.

Expression of FasL and its interaction with Fas are mediated by c-Jun N-terminal kinase (JNK) pathway in 6-OHDA-induced rat model of Parkinson disease.

Our previous studies and those of others have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in 6-hydroxydopamine (6-OHDA)-induced dopaminergic neuron injury in the substantia nigra. However, the downstream mechanism that accounts for the proapoptotic actions of JNK in 6-OHDA lesion remains to be investigated in detail. Fas, a member of the tumor necrosis factor receptor family with proapoptotic functions, was reported to be elevated within the striatum and substantia nigra pars compacta (SNc) of Parkinson's disease (PD) patients.

New protein kinase C activator regulates amyloid precursor protein processing in vitro by increasing alpha-secretase activity.

The beta amyloid (Abeta) cascade has been at the forefront of the hypothesis used to describe the pathogenesis of Alzheimer's disease (AD). It is generally accepted that drugs that can regulate the processing of the amyloid precursor protein (APP) toward the non-amyloidogenic pathway may have a therapeutic potential. Previous studies have shown that protein kinase C (PKC) hypofunction has an important role in AD pathophysiology.