Curcumin (diferuloylmethane), a polyphenol extracted from the plant Curcuma longa, is widely used in Southeast Asia, China and India in food preparation and for medicinal purposes. Since the second half of the last century, this traditional medicine has attracted the attention of scientists from multiple disciplines to elucidate its pharmacological properties. Of significant interest is curcumin’s role to treat neurodegenerative diseases including Alzheimer’s disease (AD), and Parkinson’s disease (PD) and malignancy. These diseases all share an inflammatory basis, involving increased cellular reactive oxygen species (ROS) accumulation and oxidative damage to lipids, nucleic acids and proteins. The therapeutic benefits of curcumin for these neurodegenerative diseases appear multifactorial via regulation of transcription factors, cytokines and enzymes associated with (Nuclear factor kappa beta) NFκB activity. This review describes the historical use of curcumin in medicine, its chemistry, stability and biological activities, including curcumin's anti-cancer, anti-microbial, anti-oxidant, and anti-inflammatory properties. The review further discusses the pharmacology of curcumin and provides new perspectives on its therapeutic potential and limitations. Especially, the review focuses in detail on the effectiveness of curcumin and its mechanism of actions in treating neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases and brain malignancies.

Today, there is a controversial debate in many scientific and public communities on how much sunlight is appropriate to balance between the positive and negative effects of solar UV-exposure. UV exposure undoubtedly causes DNA damage of skin cells and is a major environmental risk factor for all types of skin cancers. In geographic terms, living in parts of the world with increased erythemal UV or high average annual bright sun results in increased risks of skin cancers, with the greatest increased risk for squamous cell carcinoma, followed by basal cell carcinoma and then melanoma. On the other hand, sunlight exerts positive effects on human health, that are mediated in part via UV-B-mediated cutaneous photosynthesis of vitamin D. It has been estimated that at present, approximately 1 billion people worldwide are vitamin D-deficient or -insufficient. This epidemic causes serious health problems that are still widely under-recognized. Vitamin D deficiency leads to well documented problems for bone and muscle function. There are also associations between vitamin D-deficiency and increased incidence of and/or unfavourable outcome for a broad variety of independent diseases, including various types of malignancies (e.g. colon-, skin-, and breast cancer), autoimmune diseases, infectious diseases, and cardiovascular diseases. In this review, the present literature is analyzed to summarize our present knowledge about the important relationship of sunlight, vitamin D and skin cancer.

Despite nominally common mechanisms of action and often presumed biological equivalence, the NMDA antagonists tested produced very diverse effects on the expression of instrumental action. Other aspects of responding were left intact, including switching and matching behaviours, and the ability to respond to conditional stimuli. The implications of such findings with regard to animal modelling of schizophrenic psychotic symptoms are manifold.

A significant number of Australians are deficient in vitamin D — it is a fallacy that Australians receive adequate vitamin D from casual exposure to sunlight. People at high risk of vitamin D deficiency include elderly people (particularly those in residential care), people with skin conditions where avoidance of sunlight is advised, those with dark skin (particularly if veiled), and those with malabsorption. Exposure of hands, face and arms to one‐third of a minimal erythemal dose (MED) of sunlight (the amount that produces a faint redness of skin) most days is recommended for adequate endogenous vitamin D synthesis. However, deliberate sun exposure between 10:00 and 14:00 in summer (11:00–15:00 daylight saving time) is not advised. If this sun exposure is not possible, then a vitamin D supplement of at least 400 IU (10 μg) per day is recommended. In vitamin D deficiency, supplementation with 3000–5000 IU ergocalciferol per day (Ostelin [Boots]; 3–5 capsules per day) for 6–12 weeks is recommended. Larger‐dose preparations of ergocalciferol or cholecalciferol are available in New Zealand, Asia and the United States and would be useful in Australia to treat moderate to severe vitamin D deficiency states in the elderly and those with poor absorption; one or two annual intramuscular doses of 300 000 IU of cholecalciferol have been shown to reverse vitamin D deficiency states.