Research Updates

New Studies Affirm Tau's Infectious Spread

Cure Alzheimer’s Fund a Longtime Supporter of Tau Research

by Rudy Tanzi

Targretin Fails: High Hopes Dashed for a New Treatment for Alzheimer’s

While many were anxious to accept initial findings showing a drug known as Targretin’s “too good to be true” lab results with Alzheimer’s disease, subsequent attempts to confirm and replicate the original data regarding the ability of Targretin to remove amyloid plaques, the cardinal lesion of the disease,  have largely failed. Cure Alzheimer’s Fund Research Consortium members Dr.

Public/Private Funding of Research on Alzheimer's Disease Guides Drug Discovery

Cure Alzheimer’s Fund and National Institute of Mental Health Join in Awarding Millions for Whole Genome Sequencing

New Research Co-Funded by Cure Alzheimer’s Fund Shows New Alzheimer’s Gene, CD33, May Hold Key to Treatment

BOSTON— Excessive levels of the protein CD33 can impede the clearance of the plaque-forming protein, amyloid beta, the key component of senile plaques in the brains of Alzheimer’s disease patients. The discovery, made by Dr. Rudolph Tanzi and colleagues at Massachusetts General Hospital, and co-funded by the Cure Alzheimer’s Fund and the National Institute of Mental Health (NIMH) will be published in the journal Neuron.

High levels of exposure to air pollution may increase the risk of Alzheimer’s disease, according to a new study completed with a grant from the Cure Alzheimer’s Fund.

The study, led by Cure Alzheimer’s Research Consortium member Sam Gandy, M.D., Ph.D., of the Icahn School of Medicine at Mount Sinai, examined how elements in air pollution such as nickel nanoparticles affect the levels of certain peptides in the brain that are found to be at heightened levels in patients suffering from Alzheimer’s Disease.

“We don’t yet completely understand why the peptides accumulate, but we do know the genes responding to the peptides play an important role in developing Alzheimer’s,” said Gandy.

Traumatic Brain Injury (TBI) can lead to Neurodegenerative Syndromes that include Alzheimer Disease (AD) and Chronic Traumatic Encephalopathy (CTE)

Traumatic Brain Injury (TBI) can lead to Neurodegenerative Syndromes that include Alzheimer Disease (AD) and Chronic Traumatic Encephalopathy (CTE)

The April issue of Nature Reviews Neurology is devoted to Traumatic Brain Injury (TBI) and Chronic Traumatic Encephalopathy (CTE). Cure Alzheimer’s Fund research consortium member, Sam Gandy, M.D., Ph.D., of the Icahn School of Medicine at Mount Sinai is senior author of the lead review and overview.

Researchers Reprogramming Skin Cells into Brain Cells to Understand Alzheimer's Disease

Collaboration with the New York Stem Cell Foundation will involve using skin samples and brain imaging to identify causes and cures

Cure Alzheimer's Funded Research: New Findings Overturn Commonly Held Views of the NMDA Receptors Creating New Targets in the Treatment of Alzheimer's Disease

Cure Alzheimer's Fund Research Consortium member RobertManilow, M.D., Ph.D., professor of neurosciences at UC San Diego School of Medicine and colleagues found that key changes to the NMDA receptor, located at neuronal synapses and associated with cognition, learning and memory, result in weakening of synapses and impaired brain function. See the full story in ScienceDaily

Cure Alzheimer’s Fund's Potential New Treatment to Stop Alzheimer's Disease: Molecular 'Tweezers' Break Up Toxic Aggregations of Proteins in Mouse Model

ScienceDaily (Nov. 15, 2012) — Last March, researchers at UCLA reported the development of a molecular compound called CLR01 that prevented toxic proteins associated with Parkinson's disease from binding together and killing the brain's neurons.

Here’s the link to the article:

Potential New Treatment to Stop Alzheimer's Disease: Molecular 'Tweezers ...

Eli Lilly Drug Slows Decline in Early-Stage Patients

October 9 -- Eli Lilly announced encouraging results yesterday involving their experimental drug Solanezumab. Solanezumab is an antibody aimed at lowering beta-amyloid levels in the brain. In trials lasting 18 months, patients with mild Alzheimer's symptoms taking Solanezumab showed significantly less cognitive decline -- 34% less -- compared with patients taking the placebo.