Pivotal study finds link between PTSD and dementia

More study needed to determine why veterans with PTSD are more at risk than others

Results of a study reported in the September issue of the Journal of the American Geriatrics Society suggest that Veterans with post-traumatic stress disorder (PTSD) have a greater risk for dementia than Veterans without PTSD, even those who suffered traumatic injuries during combat.

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Scientists identify protein that spurs formation of Alzheimer’s plaques

In Alzheimer’s disease, the problem is beta-amyloid, a protein that accumulates in the brain and causes nerve cells to weaken and die. Drugs designed to eliminate plaques made of beta-amyloid have a fatal problem: they need to enter the brain and remove the plaques without attacking healthy brain cells. New research from the laboratory of Nobel Prize winner Paul Greengard, however, suggests that treatments modeled on the blockbuster cancer drug Gleevec could be the solution. The findings are reported in the Sept. 2 issue of the journal Nature.

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Brain exercises may slow cognitive decline initially, but speed up dementia later

ST. PAUL, Minn. – New research shows that mentally stimulating activities such as crossword puzzles, reading and listening to the radio may, at first, slow the decline of thinking skills but speed up dementia later in old age. The research is published in the September 1, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology.

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Rheumatoid arthritis signaling protein reverses Alzheimer’s disease in mouse model

New study shows GM-CSF reduces AD pathology and eliminates memory loss

A signaling protein released during rheumatoid arthritis dramatically reduced Alzheimer’s disease pathology and reversed the memory impairment of mice bred to develop symptoms of the neurodegenerative disease, a new study by the University of South Florida reports. Researchers found that the protein, GM-CSF, likely stimulates the body’s natural scavenger cells to attack and remove Alzheimer’s amyloid deposits in the brain.

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Study explains why Alzheimer’s drug is both safe and effective

Sanford-Burnham scientists uncover new clues to the molecular action of memantine, a drug used to treat Alzheimer’s disease, that show why side effects are rare

Alzheimer’s disease destroys brain cells and their connections (called synapses), causing memory loss and other cognitive problems that disrupt work, hobbies and daily life. Symptoms can be alleviated, in part, by the drug memantine (marketed in the United States as Namenda), which is currently FDA-approved to treat moderate-to-severe Alzheimer’s disease and was, in part, developed by Stuart A. Lipton, M.D., Ph.D., Director of the Del E. Web Center for Neuroscience, Aging and Stem Cell Research at Sanford-Burnham Medical Research Institute (Sanford-Burnham). Memantine improves symptoms by blocking abnormal activity of glutamate, a chemical that transmits messages between nerve cells. In a study appearing August 18 in The Journal of Neuroscience, a team of investigators at Sanford-Burnham led by Dr. Lipton unravel exactly how memantine helps Alzheimer’s patients without causing serious side effects.

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Deep Brain Stimulation shows promise for patients with Alzheimer’s

In a world first, Dr. Andres M. Lozano and his team at Toronto Western Hospital has shown using Deep Brain Stimulation (DBS) on patients with early signs of Alzheimer’s disease is safe and may help improve memory.

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New evidence from NYUCD supports link between gum inflammation and Alzheimer’s disease

NYU dental researchers have found the first long-term evidence that periodontal (gum) disease may increase the risk of cognitive dysfunction associated with Alzheimer’s disease in healthy individuals as well as in those who already are cognitively impaired.

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Scientists discover how neuroglobin protects against Alzheimer’s

A team of scientists at the University of California, Davis, and the University of Auckland has discovered that neuroglobin may protect against Alzheimer’s disease by preventing brain neurons from dying in response to natural stress

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New pathway to Parkinson’s and Alzheimer’s diseases

Sanford-Burnham researchers uncover new clues about the cause of brain cell death in neurodegenerative disorders such as Parkinson’s, Alzheimer’s and Huntington’s diseases

LA JOLLA, Calif., July 29, 2010 – Although their genetic underpinnings differ, Alzheimer’s disease, Parkinson’s disease and Huntington’s disease are all characterized by the untimely death of brain cells. What triggers cell death in the brain? According to a new study published by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) in the July 30 issue of Molecular Cell, the answer in some cases is the untimely transfer of a gaseous molecule (known as nitric oxide, or NO) from one protein to another.

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Sleep disorder may signal dementia, Parkinson’s disease up to 50 years early

ST. PAUL, Minn. – A new study shows that a sleep disorder may be a sign of dementia or Parkinson’s disease up to 50 years before the disorders are diagnosed. The research is published in the July 28, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology.

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