Drug Restores Cells and Memories in Alzheimer’s: Mouse Study

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Summary: A new drug has proven effective at restoring memories and neural connections in mouse models of Alzheimer’s disease. The new drug was originally developed as a treatment for Schizophrenia. While the drug does not destroy amyloid plaques associated with Alzheimer’s, it does allow the plaques to co-exist with neurons.

Source: Yale.

A new drug can restore memories and connections between brain cells in mice with a model of Alzheimer’s disease, a new Yale-led study suggests.

“The drug completely erased evidence of Alzheimer’s synapse damage and memory loss in mouse models of the disease,” said Stephen Strittmatter, the Vincent Coates Professor of Neurology and senior author of the study appearing July 5 in the journal Cell Reports.

Researchers such as Strittmatter have made significant inroads into understanding the biology of Alzheimer’s disease, but identifying effective and safe treatments has been difficult. It is known that amyloid-beta peptides, the hallmark of Alzheimer’s, couple with prion protein at the surface of brain cells and transmit damaging instructions to the interior of the cell. Yale researchers had previously identified a protein on the cell membrane — metabotropic glutamate receptor 5 or mGluR5 — as the gateway that helps transmit damage from the coupling.

Previous attempts had been made to target mGluR5, but most drugs also disrupt signaling of glutamate, the most common neurotransmitter in the human brain. The new compound, Silent Allosteric Modulation or SAM (BMS 984923), was created by Bristol Myers Squibb as part of its effort to treat schizophrenia. The drug does not restrict neurotransmitter signaling in culture tissue or living mice, the study found. After four weeks of treatment, memory and synapses linking brain cells had been restored in mice with a model of Alzheimer’s.

“The drug does not destroy plaques associated with Alzheimer’s, but allows them to co-exist with neurons,” Strittmatter said.

Cortical tissue with plaques stained in blue, and astrocytes responding to drug treatment in red. NeuroscienceNews.com image is credited to the researchers.

Yale researchers say the next step is to prepare for preliminary trials of the drug’s effects on humans.

Primary funding for the research comes from the National Institutes of Health.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Yale’s Laura T. Haas is lead author of the study. Researchers from Bristol-Myers Squibb Research and Development also contributed to the paper.

Source: Bill Hathaway – Yale

Diabetes Drug May Restore Memory In Alzheimer's

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Medical News Today

Researchers in Canada have discovered a drug originally intended for the treatment of diabetes may restore memory in brain cells affected by Alzheimer's disease. In tests on animal brain cells, they found that AC253, a diabetes drug that never made it to market, restored memory to levels similar to those of normal cells. Trials could start in five years, should further tests succeed, says the team.

The researchers write about their work in a paper published online in The Journal of Neuroscience on 28 November.

In a statement released on Tuesday, senior author Jack Jhamandas, a researcher with the Faculty of Medicine & Dentistry at the University of Alberta, says their discovery is "very important" because:

"... it tells us that drugs like this might be able to restore memory, even after Alzheimer's disease may have set in."

Estimates suggest in the next 30 years, 1,125,000 Canadians will be diagnosed with Alzheimer's disease.

Cells of people with Alzheimer's contain amyloid protein, which is found in particularly large amounts in cells from the memory and cognition parts of the brain. It is the presence of this protein that is believed to impair memory.

Last year, Jhamandas and his team showed that AC253 could block the toxic effects of amyloid protein that lead to brain-cell death.

For this latest study, they tested: read all about a Diabetes Drug May Restore Memory In Alzheimer's

Single brain trauma affects an enzyme associated with Alzheimer's disease

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Tufts Now

By 

News Staff

A study, performed in mice and utilizing post-mortem samples of brains from patients with Alzheimer’s disease, found that a single event of a moderate-to-severe traumatic brain injury (TBI) can disrupt proteins that regulate an enzyme associated with Alzheimer’s. The paper, published in the Journal of Neuroscience, identifies the complex mechanisms that result in a rapid and robust post-injury elevation of the enzyme BACE1 in the brain. These results may lead to the development of a drug treatment that targets this mechanism to slow the progression of Alzheimer’s disease.

“A moderate-to-severe TBI, or head trauma, is one of the strongest environmental risk factors for Alzheimer’s disease. A serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1. Elevations of this enzyme cause elevated levels of amyloid-beta, the key component of brain plaques associated with senility and Alzheimer’s disease,” says first author Kendall Walker, postdoctoral associate in the department of neuroscience at Tufts University School of Medicine (TUSM). 

Moderate-to-severe TBIs are caused most often by traumas such as severe falls or motor vehicle accidents that result in a loss of consciousness. Not all traumas to the head result in a TBI. According to the Centers for Disease Control and Prevention, each year 1.7 million people sustain a TBI. Concussions, the mildest form of a TBI, account for about 75 percent of all TBIs. Studies have linked repeated head trauma to brain disease, and some previous studies have linked single events of brain trauma to brain disease, such as Alzheimer’s. Alzheimer’s disease currently affects as many as 5.1 million Americans and is the most common cause of dementia in adults age 65 and over.

Building on her previous work, Giuseppina Tesco, an assistant professor of neuroscience in the School of Medicine, led a research team that first used an in vivo model to determine how a single episode of TBI could alter the brain. In the acute phase (first two days) following injury, levels of two intracellular trafficking proteins (GGA1 and GGA3) were reduced, and an elevation of BACE1 enzyme level was observed.

Next, in an analysis of post-mortem brain samples from patients with Alzheimer’s disease, the researchers found that GGA1 and GGA3 levels were reduced while BACE1 levels were elevated in the brains of Alzheimer’s disease patients compared to the brains of people without Alzheimer’s disease, suggesting a possible inverse association.

In an additional experiment using a mouse strain genetically modified to express the reduced level of GGA3 that was observed in the brains of Alzheimer’s disease patients, the team found that one week following traumatic brain injury, BACE1 and amyloid-beta levels remained elevated even when GGA1 levels had returned to normal. The research suggests that reduced levels of GGA3 were solely responsible for the increase in BACE 1 levels and therefore the sustained amyloid-beta production observed in the sub-acute phase, or seven days, after injury.

“When the proteins are at normal levels, they work as a clean-up crew for the brain by regulating the removal of BACE1 enzymes and facilitating their transport to lysosomes within brain cells, an area of the cell that breaks down and removes excess cellular material. BACE1 enzyme levels may be stabilized when levels of the two proteins are low, likely caused by an interruption in the natural disposal process of the enzyme,” said Tesco, who is also member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.

“We found that GGA1 and GGA3 act synergistically to regulate BACE1 post-injury. The identification of this interaction may provide a drug target to therapeutically regulate the BACE1 enzyme and reduce the deposition of amyloid-beta in Alzheimer’s patients,” she continued. “Our next steps are to confirm these findings in post-mortem brain samples from patients with moderate-to-severe traumatic brain injuries.”

$2.6 Million To Develop Alzheimer's Treatment Using Umbilical Cord Blood Cells

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The National Institutes of Health has awarded a three-year, $2.6-million grant to the University of South Florida and Tampa-based biotechnology company Saneron-CCEL Therapeutics, Inc., to establish dosing and safety guidelines for transplanting human umbilical cord blood cells (HUBC) into animal models of Alzheimer's disease. The researchers hope to use the pre-clinical data to gain U.S. Food and Drug Administration approval to carry out clinical trials with patients suffering from Alzheimer's disease.

"Our immediate goal is to move our beneficial findings with cord blood cells into clinical trials for patients with mild to moderate Alzheimer's disease," said the grant's principal investigator Dr. Jun Tan, a USF neuroscientist and professor of psychiatry.

The NIH Phase II Small Business Technology Transfer grant is based on the success of an ongoing research partnership between USF and Saneron aimed at determining the therapeutic benefits HUBCs offer when transplanted into animal models of a variety of neurological diseases, including Parkinson's disease, Lou Gehrig's disease (ALS), Alzheimer's disease and stroke.

"Our next stage of research is

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