by Science Daily:

Injecting synthetic tau fibrils into animal models induces Alzheimer’s-like tau tangles and imitates the spread of tau pathology, according to research from the Perelman School of Medicine at the University of Pennsylvania being presented at the American Academy of Neurology’s 65th Annual Meeting in San Diego March 16-23, 2013.

This Alzheimer’s research, along with additional Parkinson’s research from Penn and beyond, further demonstrates the cell-to-cell transmission of neurodegenerative proteins. John Q. Trojanowski, MD, PhD, co-director of the Center for Neurodegenerative Disease Research (CNDR) and professor of Pathology and Laboratory Medicine at the Perelman School of Medicine, University of Pennsylvania, will present the research in the Hot Topics plenary session on Tuesday, March 19.

by EurekAlert:

Cycles of a normal diet and protein restriction improved memory and slowed the advance of the disease.

Mice with many of the pathologies of Alzheimer’s Disease showed fewer signs of the disease when given a protein-restricted diet supplemented with specific amino acids every other week for four months.

Mice at advanced stages of the disease were put on the new diet. They showed improved cognitive abilities over their non-dieting peers when their memory was tested using mazes. In addition, fewer of their neurons contained abnormal levels of a damaged protein, called “tau,” which accumulates in the brains of Alzheimer’s patients.

Dietary protein is the major dietary regulator of a growth hormone known as IGF-1, which has been associated with aging and diseases in mice and several diseases in older adults.

Upcoming studies by USC Professor Valter Longo, the study’s corresponding author, will attempt to determine whether humans respond similarly – while simultaneously examining the effects of dietary restrictions on cancer, diabetes and cardiac disease.

by Science Daily:

Researchers from Inserm and the Université Lille/Université Lille Nord de France have recently used a neurodegeneration model of Alzheimer’s disease to provide experimental evidence of the relationship between obesity and disorders linked to the tau protein.

This research was conducted on mice and is published in theDiabetes review: it corroborates the theory that metabolic anomalies contribute massively to the development of dementia.

In France, more than 860,000 people suffer from Alzheimer’s disease and related disorders, making them the largest cause of age-related loss of intellectual function. Cognitive impairments observed in Alzheimer’s disease result from the accumulation of abnormal tau proteins in nerve cells undergoing degeneration. We know that obesity, a major risk factor in the development of insulin resistance and type 2 diabetes, increases the risk of dementia during the aging process.

by UQ News:

Size really does matter according to scientists looking for ways to cure Alzheimer’s disease.

Research conducted by scientists at the Queensland Brain Institute (QBI) at The University of Queensland (UQ) and Harvard University, has led to the discovery that treatment for Alzheimer’s disease may lie in modifying the length of subcellular structures in the brain responsible for metabolising energy, mitochondria.

The study found in cases where the mitochondria were abnormally long, they had a toxic effect inducing cell death.

by Science Daily:

During Alzheimer’s disease, ‘plaques’ of amyloid beta (Ab) and tau protein ‘tangles’ develop in the brain, leading to the death of brain cells and disruption of chemical signaling between neurons. This leads to loss of memory, mood changes, and difficulties with reasoning.

New research published in BioMed Central’s open access journal Alzheimer’s Research & Therapy, has found that up-regulating the gene Hes1 largely counteracted the effects of Ab on neurons, including preventing cell death, and on GABAergic signaling.

The exact mechanism behind how Ab contributes to Alzheimer’s disease is not yet fully understood, however researchers from Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) in Spain recently discovered that Ab interferes with the normal activity of nerve growth factor (NGF). One of the actions of NGF is activating the protein Hes1, a transcription factor required to turn on other genes. Without this factor GABAergic signaling within the brain decreases.

by John Gever for Medpage Today:

Researchers said they were encouraged by an oral drug targeting tau deposits in Alzheimer’s disease and frontotemporal dementia, even though it failed to show clinical benefit in a 1-year trial.

The drug, a kinase inhibitor called tideglusib, significantly slowed the rate of brain atrophy in patients with progressive supranuclear palsy (PSP), a form of frontotemporal dementia, said Gunter Hoeglinger, MD, of the German Center for Neurodegenerative Diseases in Munich, Germany.

As a result, his research group and the company developing the drug remain optimistic that they are on the right track, despite missing all the prespecified clinical endpoints in the phase II trial, Hoeglinger told attendees at a late-breaking abstract session here at the Alzheimer’s Association International Conference.

PSP is a rare form of dementia, occurring in about 10 people per 100,000 in the general population. But it has a relative early average onset (mean age 63) and few patients live for as long as 10 years after diagnosis.

by Health Canal:

When Dr. Alois Alzheimer in 1906 first described the malady named after him, he called it “a peculiar disease of the cerebral cortex,” or the brain’s gray matter that regulates learning and memory.

More than a hundred years later, researchers at the University of Wisconsin School of Medicine and Public Health now believe Alzheimer’s may develop in its early stages in the brain’s “white matter,” which coordinates various functions in the central nervous system.

by Market Watch for The Wall Street Journal:

 A study by researchers at the Banner Sun Health Research Institute suggests that plasma levels of tau, a protein formed in the brain, appears to be a biomarker and a strong predictor for Alzheimer’s disease.

The study, led by Dr. Larry Speaks at the Banner Sun Health Research Institute (BSHRI), is published in the June edition of American Journal of Neurodegenerative Disease. Sparks and other researchers measured tau levels in human plasma and found “significant differences” between cognitively normal individuals and those with either mild cognitive impairment or Alzheimer’s disease. Significantly, Sparks and his team found that the levels of tau were significantly lower in plasma measured in those with diagnosed Alzheimer’s disease compared to those with no sign of cognitive decline.

read more

by Denise Grady for The New York Times

“If there’s something to be done, I want to be in on the ground floor,” said Elizabeth, 67, a woman participating in studies of frontotemporal degeneration at the University of California, San Francisco.

by Current News

Researchers at Mount Sinai School of Medicine have gained insight into the mechanism by which a pathological brain protein called tau contributes to the progression of Alzheimer’s disease (AD) and other neurodegenerative disorders. This finding, published in the most recent issue of the Journal of Biological Chemistry, may provide the basis for future investigations on how to prevent tau from damaging brain circuits involved in cognitive function.

Previous studies have shown that the abnormal folding, or misfolding, and buildup of tau are key neuropathological features of many neurodegenerative disorders, including AD. Some research has demonstrated that AD-type tau neuropathology spreads in the brain, seemingly moving from one brain cell to another.

A research group led by Giulio Maria Pasinetti, MD, PhD, Saunders Family Chair in Neurology at Mount Sinai School of Medicine, explored whether misfolded tau released by neurons from the human brain – also known as paired helical filaments (PHFs) – could actually be taken up by surrounding cells and promote the spread of tau neuropathology.