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[ Too Early To Promote Smell Test For Alzheimer's ]

Too Early To Promote Smell Test For Alzheimer's

A study published online in The Laryngoscope reveals that current studies do not support the use of olfactory identification tests (smell tests) for predicting Alzheimer's dementia. Alzheimer's is a progressive disease that causes loss of brain function and is the most common cause of dementia. The disease is expected to double every 20 years through the year 2040. The study, conducted by Robert Wood Johnson Foundation (RWJF) Clinical Scholars at the University of Michigan and the VA Center for Clinical Management Research, is the first systematic review of the quantity and quality of these tests as prognostic tools for Alzheimer's. Gordon Sun, M.D., a general otolaryngologist and RWJF/US Department of Veterans Affairs Clinical Scholar at the University of Michigan, Ann Arbor, explains: "Smell tests have been touted as a possible way of predicting Alzheimer's dementia because of a reported association with decreased sense of smell.

Alzheimer's Disease And The Mechanism Behind Tau Spreading In The Brain

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.

Discovery Of Potential Trigger For Alzheimer's Disease

A highly toxic beta-amyloid - a protein that exists in the brains of Alzheimer's disease victims - has been found to greatly increase the toxicity of other more common and less toxic beta-amyloids, serving as a possible "trigger" for the advent and development of Alzheimer's, researchers at the University of Virginia and German biotech company Probiodrug have discovered. The finding, reported in the journal Nature, could lead to more effective treatments for Alzheimer's. Already, Probiodrug AG, based in Halle, Germany has completed phase 1 clinical trials in Europe with a small molecule that inhibits an enzyme, glutaminyl cyclase, that catalyzes the formation of this hypertoxic version of beta-amyloid. "This form of beta-amyloid, called pyroglutamylated (or pyroglu) beta-amyloid, is a real bad guy in Alzheimer's disease, " said principal investigator George Bloom, a U.

Memantine Improves Some Alzheimer's Symptoms But Has No Effect On Agitation

A drug prescribed for Alzheimer's disease does not ease clinically significant agitation in patients, according to a new study conducted by researchers from the U.K., U.S. and Norway. This is the first randomized controlled trial designed to assess the effectiveness of the drug (generic name memantine) for significant agitation in Alzheimer's patients. Previous studies suggested memantine could help reduce agitation and improve cognitive functions such as memory. Led by the University of East Anglia in the U.K., the new research found that while memantine does improve cognitive functioning and neuropsychiatric symptoms such as delusion, mood and anxiety, it is no more effective in reducing significant agitation than a placebo. "Memantine is quite commonly prescribed for Alzheimer's disease in the U.

In Alzheimer's Patients, Pulse Pressure Elevation Could Presage Cerebrovascular Disease

Researchers at the University of California, San Diego and Veterans Affairs San Diego Healthcare System have shown that elevated pulse pressure may increase the risk of cerebrovascular disease (CVD) in older adults with Alzheimer's disease (AD). Their study has been published in the early online edition of Journal of Alzheimer's Disease in advance of the June 5 print publication. The findings may have treatment implications, since some antihypertensive medications specifically address the pulsatile component of blood pressure. Pulse pressure (PP) - the difference between systolic and diastolic pressure - is one measure of the pulsatile component of blood pressure. PP increases substantially with age, partially due to hardening of the arteries. Hypertension is a common risk factor for AD, but the use of antihypertensive medications to prevent dementia has had mixed results.

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