Tau Pathology is the Main Cause of Alzheimer's Disease

The progression of dysfunctional tau protein is the ultimate driver behind the cognitive decline and memory loss associated with Alzheimer's disease.

The conclusion was reached after researchers from the Mayo Clinic examined more than 3,600 brains postmortem, concluding that the build-up of amyloid aids in dementia progression, but is not a primary cause of the neurodegenerative disease.

Findings from the two-part study, which were published in Brain, suggest that stopping the spread of toxic tau protein should be a new focus in Alzheimer's research and drug development.

see More : http://www.neurologyadvisor.com/tau-pathology-alzheimers-disease/article/405445/

Lack of Sleep Promotes Alzheimer’s by Preventing Critical Detoxification

By Dr. Mercola

Sleep disturbances are endemic in the US, where nearly 40 percent of adults report unintentionally falling asleep during the day in the past month, and five percent report nodding off while driving.1

Forty-five percent of teens also don't get enough sleep on school nights and 25 percent report falling asleep in class at least once a week.

Lack of sleep has ramifications that go far beyond not feeling fully awake and refreshed during the day. There's a price to pay in terms of health, both short- and long-term.

A number of studies have linked poor sleep or lack of sleep to an increased risk of Alzheimer's for example, and one of the reasons for this has to do with the fact that your brain's waste removal system only operates during deep sleep.

see more :http://articles.mercola.com/sites/articles/archive/2015/04/02/poor-sleep-promotes-alzheimers.aspx

Reinstatement of long-term memory following erasure of its behavioral and synaptic expression inAplysia

Long-term memory (LTM) is believed to be stored in the brain as changes in synaptic connections. Here, we show that LTM storage and synaptic change can be dissociated. Cocultures of Aplysiasensory and motor neurons were trained with spaced pulses of serotonin, which induces long-term facilitation. Serotonin (5HT) triggered growth of new presynaptic varicosities, a synaptic mechanism of long-term sensitization. Following 5HT training, two antimnemonic treatments—reconsolidation blockade and inhibition of PKM—caused the number of presynaptic varicosities to revert to the original, pretraining value. Surprisingly, the final synaptic structure was not achieved by targeted retraction of the 5HT-induced varicosities but, rather, by an apparently arbitrary retraction of both 5HT-induced and original synapses. In addition, we find evidence that the LTM for sensitization persists covertly after its apparent elimination by the same antimnemonic treatments that erase learning-related synaptic growth. These results challenge the idea that stable synapses store long-term memories.

see more: http://elifesciences.org/content/3/e03896

http://www.iflscience.com/brain/long-term-memories-may-not-be-stored-synapses-afterall

Nerium Acquires Anti-Aging Molecule SIG-1273 Skin.

Nerium International has obtained the world-wide exclusive rights to the patented SIG-1273® anti-aging molecule engineered by Princeton University biochemist Jeffry Stock. SIG-1273 is the result of 20 years of intensive biomedical skin care research. This intelligent molecule was perfected and patented as SIG-1273 after the creation and study of 1,272 preliminary molecules. This revolutionary anti-aging molecule with superior age-defying benefits is now available exclusively in Nerium International’s Optimera Formula line.

http://www.neriumblog.net/announcements/sig1273-anti-aging-molecule/