LATEST NEWS UPDATES
Update August 16, 2016 --Diet and exercise can reduce protein build-ups linked to Alzheimers
..."A healthy diet, regular physical activity and a normal body mass index can reduce the incidence of protein build-ups that are associated with the onset of Alzheimer's disease, research shows". See more.
Update July 25, 2016 --Antibiotic-induced perturbations in gut microbial diversity influences neuro-inflammation and amyloidosis in a murine model of Alzheimer’s disease
..."We show that prolonged shifts in gut microbial composition and diversity induced by long-term broad-spectrum combinatorial antibiotic treatment regime decreases Aβ plaque deposition...These findings suggest the gut microbiota community diversity can regulate host innate immunity mechanisms that impact Aβ amyloidosis.. Abstract and Article
Update March 18, 2016 --Tryptophan-2,3-dioxygenase (TDO) inhibition ameliorates neurodegeneration by modulation of kynurenine pathway metabolites
Genetic inhibition of two KP enzymes—kynurenine-3-monooxygenase and tryptophan-2,3-dioxygenase (TDO)—improved neurodegeneration and other disease symptoms in fruit fly models of AD, PD, and HD, and that alterations in levels of neuroactive KP metabolites likely underlie the beneficial effects. Furthermore, it was found that inhibition of TDO using a drug-like compound reverses several disease phenotypes, underscoring the therapeutic promise of targeting this pathway in neurodegenerative disease... See Article in PNAS).
Update November 14, 2015 --Experimental drug J147 targeting Alzheimer's disease shows anti-aging effects
The Salk team expanded upon their previous development of a drug candidate, called J147 (see information and molecular structure of J147) , which takes a different tack by targeting Alzheimer's major risk factor–old age. In the new work, the team showed that the drug candidate worked well in a mouse model of aging not typically used in Alzheimer's research. When these mice were treated with J147, they had better memory and cognition, healthier blood vessels in the brain and other improved physiological features, as detailed. Salk Institute says Human Trials to begin in 2016. Journal Aging November 12, 2015 in the See previous research-- Abstract.. Full Article...The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease mice --
Update July 20, 2015 --Novel antibodies show promise for Alzheimer's disease treatment--
NeuroPhage's NPT088 --Universally Targets Misfolded Proteins in Preclinical Studies Highlighted in Oral Session at the Alzheimer's Association International Conference-- (Fusion Protein -- antibody--) -- See The Virus that could cure Alzheimers.
See also: Scientists at NYU have evidence that monoclonal antibodies they developed may provide the blueprint for effective treatments for Alzheimer's disease and other neurodegenerative diseases, such as Parkinson's disease. Read news release
Update June 11,2015 --Axovant goes publc --main product candidate, RVT-101, aims to treat dementia in patients with Alzheimer’s disease --
RVT-101 has demonstrated statistically significant results on cognition as measured by the ADAS-cog and on function as measured by the ADCS-ADL in a randomized, placebo-controlled 684-subject study spanning 48 weeks of therapy, administered once-daily on a background of stable donepezil therapy. RVT-101 was well-tolerated by subjects in all 13 clinical trials conducted by GSK. We intend to commence a confirmatory phase 3 study in 2015.
Update Sept 11,2014 --In mouse model of Alzheimer's disease, targeted immune booster removes toxic proteins
Alzheimer's disease experts at NYU Langone Medical Center and elsewhere are reporting success in specifically harnessing a mouse's immune system to attack and remove the buildup of toxic proteins in the brain that are markers of the deadly neurodegenerative disease. Researchers say the immune booster reduced both amyloid beta plaques and tau tangles. Clinical Trial could begin in 2015... see full text of news release see Abstract of study.
Update August 22, 2014 - Creating
pomegranate drug to stem Alzheimer's, Parkinson's
Research will look to produce compound derivatives of punicalagin for a drug that would treat neuro-inflammation and slow down the progression of Alzheimer's disease, scientists report. see Abstract in Molecular Nutrition
New Update Jan 2014 --Dominantly Inherited Alzheimer Network Trial: An Opportunity to Prevent Dementia (DIAN TU)
This international study will assess the safety, tolerability, and biomarker efficacy of the drugs gantenerumab and solanezumab in individuals who have a genetic mutation for autosomal-dominant Alzheimer's disease. see full text
New Update -- June 18, 2013 ---Reversing the loss of brain connections in Alzheimer’s disease -
A New Drug --NitroMemantine-- Reverses Loss of Brain Connections in Alzheimer's by shutting down hyperactive eNMDA receptors on diseased neurons, NitroMemantine restores synapses between those neurons...."The Food and Drug Administration-approved drug memantine offers some beneficial effect, but the improved eNMDAR antagonist NitroMemantine completely ameliorates Aß-induced synaptic loss, providing hope for disease-modifying intervention in AD. "..- See abstract in PNAS.New Update - March 26, 2012 --PLoS ONE Journal Publishes Mechanistic Model of Alzheimer's Disease Endorsing Prana's PBT2 .
"This paper builds on Prana’s previously published findings that as we age our ability to maintain normal zinc distribution deteriorates. Abeta forms amyloid by capturing and holding zinc, which in turn further reduces our ability to maintain normal zinc distribution. “This is a vicious pathological cycle. PBT2 interrupts this cycle, re-distributing zinc needed for healthy brain function..”
See Full Article: The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease.
Update March 31, 2016 Possibility of curbing synapse loss in Alzheimer's--Targetable immune pathway plays an early role in Alzheimer's disease models, before plaque accumulation
..."Researchers show how brain connections, or synapses, are lost early in Alzheimer's disease and demonstrate that the process starts -- and could potentially be halted -- before telltale plaques accumulate in the brain." more
New Update - March 13, 2012 Potential Alzheimer's Disease Drug Slows Damage and Symptoms in Animal Model
A compound that previously progressed to Phase II clinical trials for cancer treatment slows neurological damage and improves brain function in an animal model of Alzheimer's disease, according to a new study. Summary from ScienceDaily
The Microtubule-Stabilizing Agent, Epothilone D, Reduces Axonal Dysfunction, Neurotoxicity, Cognitive Deficits, and Alzheimer-Like Pathology in an Interventional Study with Aged Tau Transgenic Mice
New Update - February 14, 2012 --Turmeric-Based Drug Effective On Alzheimer Flies
"Curcumin, a substance extracted from turmeric, prolongs life and enhances activity of fruit flies with a nervous disorder similar to Alzheimers, according to new research. The study conducted at Linköping University, indicates that it is the initial stages of fibril formation and fragments of the amyloid fibrils that are most toxic to neurons..." Summary from ScienceDaily
Source: Curcumin Promotes A-beta Fibrillation and Reduces Neurotoxicity in Transgenic Drosophila
**New Update February 9, 2012 --Alzheimer's Disease Symptoms Reversed in Mice --The cancer drug bexarotene given to mice eliminates brain-damaging proteins, leading to improved cognition.
The cancer drug was given to mice and eliminated brain-damaging proteins, leading to improved cognition within days, but it is not known if it will work in humans. See review article in Scientific American Online
**New Update -- December 12, 2011 --The Journal of Biological Chemistry published a study offering powerful validation of PBT2 as a treatment for a number of neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntingtons diseases
PBT2 is Prana Biotechnology's lead drug for treating dementia in Alzheimer's and Huntington's disease. It is a specific type of 8-OHQ. Prana designed and selected PBT2 therapy for its enhanced efficacy and tolerability.
See the full publication: , "Different 8-OHQ's Protect Models of TDP-43, alpha-synuclein, and Polyglutamine Proteotoxicity through Distinct Mechanisms".
***New Update -- December 14, 2011 --Alzheimer's drug candidate may be first to prevent disease progression Salk scientists develop new drug that improves memory and prevents brain damage in mice --
A new drug candidate may be the first capable of halting the devastating mental decline of Alzheimer's disease, based on the findings of a study published today in PLoS one. When given to mice with Alzheimer's, the drug, known as J147, improved memory and prevented brain damage caused by the disease. The new compound, developed by scientists at the Salk Institute for Biological Studies, could be tested for treatment of the disease in humans in the near future. "J147 enhances memory in both normal and Alzheimer's mice and also protects the brain from the loss of synaptic connections," says David Schubert, the head of Salk's Cellular Neurobiology Laboratory, whose team developed the new drug. "No drugs on the market for Alzheimer's have both of these properties." Although it is yet unknown whether the compound will prove safe and effective in humans, the Salk researchers' say their results suggest the drug may hold potential for treatment of people with Alzheimer's. read more...
New Update Novemember 29,2011 Surprisingly Few U.S. Physicians and Payers Surveyed Are Familiar with Late-Stage Emerging Alzheimer's Disease Therapies -- Resources, one of the world's leading research and advisory firms for pharmaceutical and healthcare issues, finds that, in the United States, surprisingly few surveyed neurologists are familiar with key emerging therapies for Alzheimer's disease on which they were surveyed.Less than one-quarter of surveyed neurologists were familiar with the anti-beta-amyloid monoclonal antibodies solanezumab (Eli Lilly) and bapineuzumab (Janssen Alzheimer Immunotherapy/Pfizer) and less than 10 percent of PCPs were familiar with these emerging disease-modifying drugs. .. read more
New Update March 3, 2011 Scripps Research study points to liver, not brain, as origin of Alzheimer's plaques
Unexpected results from a Scripps Research Institute and ModGene, LLC study could completely alter scientists' ideas about Alzheimer's disease—pointing to the liver instead of the brain as the source of the "amyloid" that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment. read more
New Update Jan 27, 2011 Stimulating The Brain's Immune Response May Provide Treatment For Alzheimer's Disease
A new target for the prevention of adverse immune responses identified as factors in the development of Alzheimer's disease (AD) has been discovered by researchers at the University of South Florida's Department of Psychiatry and the Center of Excellence for Aging and Brain Repair. read more
New Update Jan 6, 2011 -- Blood Test for Alzheimers
Using a new technology that relies on thousands of synthetic molecules to fish for disease-specific antibodies, researchers have developed a potential method for detecting Alzheimer's disease with a simple blood test. The same methodology might lead to blood tests for many important diseases, according to the report in the January 7th issue of the journal Cell, a Cell Press publication. read more
New Update -- Jan 8 2010 --New approach to fighting Alzheimer's shows potential in clinical trial Nutrient mix shows promise in improving memory
In a clinical trial of 225 Alzheimer's patients, researchers found that a cocktail of three naturally occurring nutrients believed to promote growth of those connections, known as synapses, plus other ingredients (B vitamins, phosopholipids and antioxidants), improved verbal memory in patients with mild Alzheimer's. -- read more
New Update Oct. 16, 2009 -- IL-6 (Interleukin-6) shown to remove plaque from Alzheimer's mouse model
Published online in The FASEB Journal, data is based on the unexpected finding that when the brain's immune cells (microglia) are activated by the interleukin-6 protein (IL-6), they actually remove plaques instead of causing them or making them worse. read Abstract (Massive gliosis induced by interleukin-6 suppresses A deposition in vivo: evidence against inflammation as a driving force for amyloid deposition Paramita Chakrabarty, Karen Jansen-West, Amanda Beccard, Carolina Ceballos-Diaz, Yona Levites, Christophe Verbeeck, Abba C. Zubair, Dennis Dickson, Todd E. Golde, and Pritam Das)
New Update Jul 15, 2009 Significant Increase in Overall Executive Function With PBT2
The presentation was entitled "PBT2 ameliorates cognitive impairment in Alzheimer's disease transgenic and aged mice: Evidence for a common mechanism of action." New data indicates PBT2 benefits not only Alzheimer's disease patients, but also could treat the cognitive loss commonly associated with the normal ageing process. PBT2 lowers amyloid burden in the brain and also corrects metal imbalances that occur in the aged brain. Plans for PBT2 to Advance to Phase IIb Clinical Trial Testing. See News Release.
New Update April 16, 2009 -- Depletion of circulating SAP and , almost complete, disappearance of SAP from the CSF
Here, in this unique study in Alzheimer's disease from the Journal PNAS, the bis(d-proline) compound, (R)-1-[6-[(R)-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl]pyrrolidine-2-carboxylic acid (CPHPC), was shown to deplete circulating SAP and almost complete, disappearance of SAP from the CSF. Kolstoe et.al., demonstrate that SAP depletion in vivo is caused by CPHPC cross-linking pairs of SAP molecules in solution to form complexes that are immediately cleared from the plasma. Article Title: Molecular dissection of Alzheimer's disease neuropathology by depletion of serum amyloid P component, See Abstract.
Note: Pentraxin Therapeutics Ltd, has acquired the full rights to CPHC. In February 2009 Pentraxin Therapeutics Ltd licensed CPHPC to GlaxoSmithKline for treatment of systemic amyloidosis, a rare fatal disease.