Investigating pathological mechanisms of depression as risk factors for Alzheimer's disease

Free Paper PresentationConference Theme: Brain and the Environmentpublished_or_final_versio

Neuroprotection in glaucoma using Gouqizi (Wolfberry)

Aging is an important risk factor for various neurodegenerative diseases such as glaucoma and Alzheimer's disease (AD). Glaucoma is a common eye disease that may lead to irreversible blindness. Recent studies suggest that development of anti-aging drugs from Chinese medicinal herbs may be one of the possible interventions. The fruits of Lycium barbarum (or commonly known as Gou Qi Zi, or wolfberry), has been used for thousands of years in China and is believed to be effective as an anti-aging agent as well as nourishment of eyes, livers and kidneys. We have shown that aqueous extract of wolfberry provides neuroprotection to the eyes against degeneration in an experimental model of glaucoma.published_or_final_versio

Molecular mechanism of neuroprotection in glaucoma using gouqizi (wolfberry)

published_or_final_version首都醫科大學眼科學院2009年學術年會, 北京, 2009年10月9日-10月11日. In 首都醫科大學眼科學院2009年學術年會會議指南, 2009, p. 1

Modulation of mitochondrial calcium as a pharmacological target for Alzheimer's disease

Perturbed neuronal calcium homeostasis is a prominent feature in Alzheimer's disease (AD). Mitochondria accumulate calcium ions (Ca2+) for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell. Excessive Ca2+ uptake into mitochondria often leads to mitochondrial membrane permeabilization and induction of apoptosis. Ca2+ is an interesting second messenger which can initiate both cellular life and death pathways in mitochondria. This review critically discusses the potential of manipulating mitochondrial Ca2+ concentrations as a novel therapeutic opportunity for treating AD. This review also highlights the neuroprotective role of a number of currently available agents that modulate different mitochondrial Ca2+ transport pathways. It is reasoned that these mitochondrial Ca2+ modulators are most effective in combination with agents that increase the Ca2+ buffering capacity of mitochondria. Modulation of mitochondrial Ca2+ handling is a potential pharmacological target for future development of AD treatments. © 2010 Elsevier B.V.postprin

從醫學基礎研究到保健產品談老年癡呆症：你我知多少？

http://library.hku.hk/record=b4378464published_or_final_versio

Research strategies in molecular signaling of neuronal apoptosis in Alzheimer's disease

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Viscoelastic response of neural cells governed by the deposition of amyloid-ß peptides (Aß)

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Reducing calcium-mediated endoplasmic reticulum stress could attenuate beta-amyloid peptide neurotoxicity

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From small to big molecules: how do we prevent and delay the progression of age-related neurodegeneration?

Age-related neurodegeneration in the brain and retina is complicated. It comprises a series of events encompassing different modes of degeneration in neurons, as well as inflammation mediated by glial cells. Systemic inflammation and risk factors can contribute to disease progression. Age-related conditions such as Alzheimer's disease (AD), Parkinson's disease (PD) and Age-related Macular Degeneration (AMD) affect patients for 5 to 20 years and are highly associated with risk factors such as hyperhomocysteinaemia, hypercholesterolaemia, hypertension, and symptoms of mood disorder. The long duration of the degeneration and the wide array of systemic factors provide the opportunity for nutraceutical intervention to prevent or delay disease progression. Small molecules such as phenolic compounds are candidates for neuroprotection because they have anti-oxidant activities and can modulate intracellular signaling pathways. Bigger entities such as oligosaccharides and polysaccharides have often been neglected because of their complex structure. However, certain big molecules can provide neuroprotective effects. They may also have a wide spectrum of action against risk factors. In this review we use an integrative approach to the potential uses of nutraceutical products to prevent age-related neurodegeneration. These include direct effects of phenolic compounds and polysaccharides on neurons to antagonize various neurodegenerative mechanisms in AD, PD and AMD, and indirect effects of these compounds on peripheral disease-related risk factors.postprin

Advances in Alzheimer's disease: from bench to bedside

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