Intellect Neurosciences Inc. (fka ILNS)

[montanus]

"Our lead program, CONJUMAB-A, offers an important advantage to the Aß antibodies currently in clinical development for both AD and AMD by several large pharmaceutical companies. This is because those antibodies (e.g. solanezumab, bapineuzumab, gantenerumab, crenzeumab, RN6G and GSK33766A) are designed for a single purpose, namely to clear Aß, while none act on the important secondary neurotoxic mechanisms, such as oxidative stress that causes most of the damage from Aß. By contrast, CONJUMAB-A is empowered with a potent antioxidant. An important step in establishing proof-of-principle was the initial data generated through our collaboration with iNovacia to evaluate compounds synthesized by Lonza for Intellect. The data demonstrated the conjugation of the antioxidant molecule to an amino acid does not reduce its antioxidant activity. Pending adequate financial resources, these studies, which are almost complete, will allow us to select a drug candidate to take into development, providing the trigger for us to move forward with LONZA into an expanded manufacturing project, bringing us closer to the submission of an Investigational New Drug application."

http://finance.yahoo.com/news/intellect-neurosciences-issues-letter-shareholders-173223118.html

"Traditionally, ADCs have been used to deliver a cytotoxic payload to kill cancer cells. By contrast, drugs based on CONJUMAB are comprised of antibodies targeting amyloidogenic polypeptides that would be linked chemically to a small molecule that is non-toxic and instead confers cytoprotective properties such as an antioxidant or anti-inflammatory molecule. CONJUMAB-A is comprised of a humanized monoclonal antibody against beta amyloid (Aß) conjugated to melatonin, a potent antioxidant molecule with anti-amyloidogenic, anti-inflammatory and anti-apoptotic properties with the aim of preventing the accumulation of toxic Aß in the retina and delivering on-site neuroprotection to reduce geographical atrophy and neovascularization."

http://finance.yahoo.com/news/intellect-neurosciences-present-bio-europe-143500108.html

"When amyloid is removed from brains using vaccines, it doesn't help patients. In fact, patients got slightly worse. This is true in all the studies. Further, when one sees amyloid deposition in the brain, oxidative damage decreases. So there's an inverse correlation. Whether oligomers or fibers, when we see amyloid increased, we see a decrease in the levels of oxidative damage."

http://archive.sciencewatch.com/ana/st/alz2/11junSTAlz2Perr/


Linking Poor Sleep and Alzheimer's
March 23, 2013

Alzheimers linked to poor sleep prior to cognitive problems
(dailyRx News) Poor sleep is linked to a wide range of possible ailments. However, it also works the other way around. Poor sleep can also be a sign that illness is contributing to the bad sleep.

In a recent study, researchers found that individuals with certain proteins in their spinal fluid had poor sleep quality, but not sleep quantity.

These findings suggest that poor sleep could be one symptom indicating possible development of Alzheimer's disease.

This finding does not mean that someone sleeping poorly has Alzheimer's. It means those with a risk of Alzheimer's might want to talk to a doctor if they notice their sleep quality changes.

"Talk to your doctor about sleeping problems."
The study, led by Yo-El S. Ju, MD, of the Department of Neurology at the Washington University School of Medicine in St. Louis, Missouri, aimed to discover whether changes in sleeping patterns might be related to symptoms of Alzheimer's disease.

The researchers tracked the sleep patterns of 145 individuals, all aged 45 and older, including 62 with at least one parent who developed late-onset Alzheimer's disease.

For two weeks, the participants wore actigraphs, devices that tracked their sleep and wake times. The researchers tracked how much time the participants slept in total and the quality of their sleep, based on how much time they spent in bed asleep.

The participants also kept sleep diaries to confirm the numbers and to note any naps.

Then, the researchers took samples of the participants' spinal fluid to look for evidence of beta-amyloid. Beta-amyloid is a molecule that indicates the likely development of Alzheimer's disease.

The researchers found beta-amyloid in 23 percent of the participants (32 individuals). The researchers then compared these individuals' sleep patterns with the patterns of those without beta-amyloid.

The participants with beta-amyloid deposits in their spinal fluid had worse sleep quality than those who did not have the amyloid deposits, though by only a small amount.

The sleep efficiency of those with the beta-amyloid deposits was about 80.4 percent. The sleep efficiency of those without the deposits was about 83.7 percent.

In particular, those who had sleep quality/efficiency percentages below 75 percent were more than five times more likely to have "preclinical" Alzheimer's disease.

"Preclinical" refers to having the deposits but not showing outward symptoms of the disease.

These differences held true after the researchers made adjustments to account for the participants' age and sex and whether the participants carried a particular genetic marker for Alzheimer's.

The total amount of sleep among the participants was not different, regardless of whether they had beta-amyloid deposits or not.

However, 31 percent of those with the deposits took naps three or more days a week, compared to only 15 percent of those who did not have the deposits.

The researchers therefore concluded that having beta-amyloid deposits – which indicates an early stage of Alzheimer's disease before the clinical symptoms of cognitive problems show up – is associated with poor sleep. However, having the deposits is not linked to getting less sleep.

The study was published March 11 in the journal JAMA Neurology. The research was funded by the National Institutes of Health and the Ellison Medical Foundation Senior Scholar Award.

One author has consulted for Jazz Pharmaceuticals and received research support from UCB. Another author is involved in clinical trials related to medications for dementia which are sponsored by Janssen Alzheimer Immunotherapy Program and Pfizer. He has also received consulting or speaking fees from seven other pharmaceutical companies.

http://www.dailyrx.com/alzheimers-linked-poor-sleep-prior-cognitive-problems