The Experts below are selected from a list of 84 Experts worldwide ranked by ideXlab platform

Xican Tang - One of the best experts on this subject based on the ideXlab platform.

  • progress in studies of huperzine a a natural cholinesterase inhibitor from chinese herbal medicine
    Acta Pharmacologica Sinica, 2006
    Co-Authors: Rui Wang, Han Yan, Xican Tang
    Abstract:

    Huperzine A (HupA), a novel alkaloid isolated from the Chinese herb Huperzia serrata, is a potent, highly specific and reversible inhibitor of acetylcholinesterase(AChE). Compared with tacrine, donepezil, and rivastigmine, HupA has better penetration through the blood-brain barrier, higher oral bioavailability, and longer duration of AChE inhibitory action. HupA has been found to improve cognitive deficits in a broad range of animal models. HupA possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis. These protective effects are related to its ability to attenuate oxidative stress, regulate the expression of apoptotic proteins Bcl-2, Bax, P53, and caspase-3, protect mitochondria, upregulate nerve growth factor and its receptors, and interfere with amyloid precursor protein metabolism. Antagonizing effects of HupA on N-methyl-D-aspartate receptors and potassium currents may also contribute to its neuroprotection as well. Pharmacokinetic studies in rodents, canines, and healthy human volunteers indicated that HupA was absorbed rapidly, distributed widely in the body, and eliminated at a moderate rate with the property of slow and prolonged release after oral administration. Animal and clinical safety tests showed that HupA had no unexpected toxicity, particularly the dose-limiting hepatotoxicity induced by tacrine. The phase IV clinical trials in China have demonstrated that HupA significantly improved memory deficits in elderly people with Benign Senescent Forgetfulness, and patients with Alzheimer disease and vascular dementia, with minimal peripheral cholinergic side effects and no unexpected toxicity. HupA can also be used as a protective agent against organophosphate intoxication.

Jeremia Heinik - One of the best experts on this subject based on the ideXlab platform.

  • V. A. Kral and the origins of Benign Senescent Forgetfulness and mild cognitive impairment.
    International psychogeriatrics, 2010
    Co-Authors: Jeremia Heinik
    Abstract:

    Background: The concept of Benign Senescent Forgetfulness (BSF) was introduced in 1958 by V. A. Kral, consultant neuropsychiatrist to the Montreal Hebrew Old People's and Sheltering Home (hereafter the Home). BSF was criticized and mild cognitive impairment (MCI) was adopted years later. In this paper I argue that a notion of MCI also originated with Kral. Methods: A historical review was undertaken of the Canadian Jewish Congress archives in Montreal, Kral's biography and his publications, as well as relevant literature. A discussion was held with one of Kral's collaborators. Results: In the mid-1950s the administration of the Home sought research-derived recommendations to improve residents’ conditions. In an initial survey, based on a meticulous neuropsychiatric examination, Kral departed from contemporaneous psychiatric nosology and suggested other criteria in order to classify the home's population. He classified one of the five groups, consisting of subjects with mild memory dysfunction, as having BSF. In his next survey, Kral included psychological tests in addition to clinical assessment and focused on the elderly people who were well preserved (good personal and social functioning). This sample was subdivided into four subgroups, including BSF and incipient amnestic syndrome (IAS). The findings revealed: well-preserved aged people; normal (dull) level of general intelligence; subnormal performance of specific memory and perceptual/organization tests; and no significant signs of malignant amnestic syndrome. This construct is very similar to that of MCI, which is widely used today. Conclusions: The interaction between Kral and a particular home for the elderly at a particular moment in its history gave rise to the concept of BSF, and a notion of what we now call MCI emerged.

  • V. A. Kral, the Montreal Hebrew Old People's Home, and Benign Senescent Forgetfulness
    History of Psychiatry, 2006
    Co-Authors: Jeremia Heinik
    Abstract:

    The term Benign Senescent Forgetfulness, introduced in 1958 by V. A. Kral, constitutes the origin of the concept of Mild Cognitive Impairment (MCI), a widely studied but controversial entity. The ambiguities surrounding MCI warrant a re-assessment of its historical origin. Any attempt at an in-depth investigation of Kral's works on that subject should begin with a description of the patient population and professional arena in the Montreal Hebrew Old People's and Sheltering Home, where Kral was a consultant. Based on archival and published sources, I describe the Home's facilities, population, staff and programmes/services, followed by an overview of the dynamic factors inducing a re-examination of its mode of operation in the mid-1950s when Kral joined the Home's professional staff as a consultant.

Rui Wang - One of the best experts on this subject based on the ideXlab platform.

  • progress in studies of huperzine a a natural cholinesterase inhibitor from chinese herbal medicine
    Acta Pharmacologica Sinica, 2006
    Co-Authors: Rui Wang, Han Yan, Xican Tang
    Abstract:

    Huperzine A (HupA), a novel alkaloid isolated from the Chinese herb Huperzia serrata, is a potent, highly specific and reversible inhibitor of acetylcholinesterase(AChE). Compared with tacrine, donepezil, and rivastigmine, HupA has better penetration through the blood-brain barrier, higher oral bioavailability, and longer duration of AChE inhibitory action. HupA has been found to improve cognitive deficits in a broad range of animal models. HupA possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis. These protective effects are related to its ability to attenuate oxidative stress, regulate the expression of apoptotic proteins Bcl-2, Bax, P53, and caspase-3, protect mitochondria, upregulate nerve growth factor and its receptors, and interfere with amyloid precursor protein metabolism. Antagonizing effects of HupA on N-methyl-D-aspartate receptors and potassium currents may also contribute to its neuroprotection as well. Pharmacokinetic studies in rodents, canines, and healthy human volunteers indicated that HupA was absorbed rapidly, distributed widely in the body, and eliminated at a moderate rate with the property of slow and prolonged release after oral administration. Animal and clinical safety tests showed that HupA had no unexpected toxicity, particularly the dose-limiting hepatotoxicity induced by tacrine. The phase IV clinical trials in China have demonstrated that HupA significantly improved memory deficits in elderly people with Benign Senescent Forgetfulness, and patients with Alzheimer disease and vascular dementia, with minimal peripheral cholinergic side effects and no unexpected toxicity. HupA can also be used as a protective agent against organophosphate intoxication.

Raymond Levy - One of the best experts on this subject based on the ideXlab platform.

  • Do subjective memory complaints precede dementia? A three-year follow-up of patients with supposed ‘Benign Senescent Forgetfulness’
    International Journal of Geriatric Psychiatry, 1992
    Co-Authors: John T. O'brien, Barbara Beats, Katie Hill, Robert Howard, Barbara J. Sahakian, Raymond Levy
    Abstract:

    A three-year follow-up study is reported of people presenting to a hospital memory clinic with ‘Benign Senescent Forgetfulness’.All were complaining of Forgetfulness for which no organic or psychiatric cause could be found. Sixty-four out of the 68 patients initially seen were traced, of whom three had died. Six (8.8%) were found to have become demented, a slightly higher proportion than would be expected given the age of the population. No particular clinical features were found that predicted the subsequent development of dementia. Cognitive performance of remaining non-demented subjects showed a significant but relatively modest decline, probably related to the effects of normal ageing. It is concluded that memory complaint must be taken seriously in the elderly and may sometimes indicate early dementia despite normal scores on simple screening tests. However, a finding of normality after careful assessment is reassuringly correct in the majority of cases.

J. S. Snowden - One of the best experts on this subject based on the ideXlab platform.

  • MILD COGNITIVE IMPAIRMENT: AGING TO ALZHEIMER’S DISEASE
    Brain, 2004
    Co-Authors: J. S. Snowden
    Abstract:

    MILD COGNITIVE IMPAIRMENT: AGING TO ALZHEIMER’S DISEASE Edited by Ronald C. Petersen 2003. Oxford: Oxford University Press Price: £39.50. ISBN 0‐19‐512342‐5 This is an interesting, thought‐provoking, sometimes controversial and eminently readable book. Mild cognitive impairment (MCI) refers to the borderland between normal ageing and dementia. The term MCI has recent origins, having been introduced only in the last decade in recognition of the fact that the onset of dementia is insidious. There is a prodromal phase during which an individual functions at a lower level than normal, yet the changes in cognition are insufficient to warrant a classification of dementia. Herein lies a fundamental conceptual difference between MCI and descriptive labels that acquired prominence in earlier decades, such as ‘Benign Senescent Forgetfulness’ and ‘age‐associated memory impairment’. These latter terms implied changes in memory, which were thought to be largely consistent with and the product of normal ageing. MCI, by contrast, is construed as abnormal ageing and commonly thought of as the prodrome to dementia, more specifically to Alzheimer’s disease. MCI raises a variety of conceptual issues. If MCI is cognitive impairment in excess of that expected in normal ageing, what is the yardstick for defining normal ageing? Within a lifetime, a variety of adverse events, lifestyle factors and age‐related medical conditions might potentially influence cognitive function. Studies of ‘normal’ ageing that adopt a rigorous policy of excluding from the study sample people with any potential risk factor whatever (e.g. the presence of diabetes or a history of alcohol consumption) risk identifying a population of ‘supernormals’ whose performance is unrepresentative of the ageing population as a whole. The implication of an overly …