Alzheimer’s disease may kill as many as cancer in US

Deaths from Alzheimer’s disease are under-reported in the United States and the most common form of dementia may be taking as many lives as heart disease or cancer.

Alzheimer’s disease currently ranks sixth among causes of death in the United States, according to the Centers for Disease Control and Prevention. Heart disease is first, and cancer second.

But researchers reported in the journal Neurology, the medical journal of the American Academy of Neurology, that Alzheimer’s-linked deaths could be six times more common than thought.

“Alzheimer’s disease and other dementias are under-reported on death certificates and medical records,” said study author Bryan James of Rush University Medical Center in Chicago.

“Death certificates often list the immediate cause of death, such as pneumonia, rather than listing dementia as an underlying cause.”

For the study, researchers followed more than 2,500 people aged 65 and older who were tested annually for dementia.

A total of 559 participants developed Alzheimer’s disease during the course of the study, and the average time span from diagnosis to death was four years.

People aged 75 to 84 who were diagnosed with Alzheimer’s were also four times more likely to die than those without it.

One third of all deaths among those aged 75 and older were attributable to Alzheimer’s disease, said the study.

According to James, the findings would translate to an estimated 503,400 deaths from Alzheimer’s in the US population over age 75 in 2010.

That figure is six times higher than the 83,494 reported by the CDC based on death certificates.

“Determining the true effects of dementia in this country is important for raising public awareness and identifying research priorities regarding this epidemic,” said James.

Source: Channel news asia


Eating barbecued, fried food linked to Alzheimer’s

A new study has revealed that eating a meat-rich diet, which has been fried, barbecued or grilled, can trigger Alzheimer’s disease and accelerate ageing.

Scientists have discovered that harmful ‘Ages’ compounds in the “Western diet” cause a build-up of a dangerous protein that forms toxic deposits which ravage the brain, the Daily Express reported.

Researchers found that the high levels of these compounds suppress a protective enzyme concerned in conditions related to brain, metabolic disease, ageing and diabetes.

The study has also found that fatty and sugary foods, like cheese, eggs, white bread, pasta and sugary pastries, cakes and biscuits could also play a part in Alzheimer’s by boosting Ages levels.

Dr Simon Ridley, head of research at Alzheimer’s Research UK, said that diabetes has previously been linked to an increased risk of dementia, and this new study provides fresh insight into some of the possible molecular processes that may link the two conditions.

Ridley added that eating a balanced diet can help lower the risk of Alzheimer’s and following a healthy lifestyle, which includes regular exercise, not smoking, and keeping blood pressure and weight in check can also be helpful.

The study was published in the journal Proceedings Of The National Academy Of Sciences.

Source:l Business standard


IMS-BHU researchers identify novel drug target for treating Alzheimer’s disease

Researchers at the Institute of Medical Sciences, Banaras Hindu University (IMS-BHU) have identified RhoA as a novel drug target in the treatment of Alzheimer’s disease. The study has been published in the FASEB Journal.

Dr Debabrata Dash, professor and head, department of biochemistry, IMS-BHU, said, “We have discovered a novel drug target of amyloid beta toxicity and Alzheimer’s disease in platelet model. We have found that amyloid beta exercises its activity on a cell through activation of a small GTP-binding protein known as RhoA. When we inhibit RhoA activity by employing pharmacological inhibitors, the toxic effects of amyloid beta are prevented. This information would have significant implications in drug development against Alzheimer’s disease.”

Alzheimer’s disease is the most common cause of cognitive decline and memory loss in the elderly. Although local deposit of a small peptide called ‘amyloid-beta’ is known to be responsible for Alzheimer pathology, the underlying molecular mechanism remains largely obscure. This is the reason why there is no effective therapy against this highly debilitating condition.

Platelets are blood cells that are responsible for stoppage of bleeding at the site of injury. Interestingly, platelets are a major source of amyloid-precursor protein in blood.

Dr Dash and co-workers (Vijay Sonkar and Paresh Kulkarni) at Banaras Hindu University have identified target molecules of amyloid-beta in cells using platelets as peripheral model of neurons.

Their study showed that amyloid-beta was able to strongly stimulate platelets leading to aggregate formation. Intravenous administration of the peptide in mouse accelerated thrombus formation in pulmonary vessels.

The effect of amyloid-beta on platelets was found to be mediated through activation of RhoA, a small GTP-binding protein responsible for cytoskeletal reorganization in cells, and that inhibition of RhoA by a specific pharmacological agent reversed the effects of amyloid-beta on platelets.

In order to understand molecular underpinnings amyloid action, researchers went further to demonstrate phosphorylation of downstream effectors of RhoA, namely MYPT1 and myosin light chain, when the cells were exposed to amyloid-beta.

According to the researchers, patients of Alzheimer’s also have clotting abnormalities, which could be explained by amyloid-beta-induced activation of platelets.

“The findings of this study thus identify RhoA as a novel drug target in the treatment of Alzheimer’s disease, and unravel the possible cause of clotting abnormalities seen in these patients,” said Dr Dash.

Sourrce: India Medical Times


Elusive Secret of HIV Long-Term Immunity

Discovery offers hope of new, shorter HIV treatment if drugs are started right away

Scientists have discovered a critical new clue about why some people are able to control the HIV virus long term without taking antiviral drugs. The finding may be useful in shortening drug treatment for everyone else with HIV.

These rare individuals who do not require medicine have an extra helping of a certain type of immune protein that blocks HIV from spreading within the body by turning it into an impotent wimp, Northwestern Medicine® scientists report. The new finding comes from analyzing cells from these rare individuals and HIV in the lab.

Scientists have been trying to solve the mystery of why 1 percent of people with HIV — called “controllers” — have enduring control of the virus without medications, in some cases for life. The controllers’ early defense against HIV is quickly extinguished by the virus, so how do they have long-term immunity? The Northwestern discovery represents what scientists have long sought: a second line of defense deep in the immune system backing up the short-lived early defense.

This discovery suggests a novel approach involving much earlier treatment that could potentially make every HIV-infected person into a controller for the long term by protecting the reserves of this defensive immune protein. The goal would be for them to eventually be free from anti-retroviral drugs.

Currently most HIV patients need to take powerful anti-retroviral drugs every single day for life. If the medicines are stopped, the virus quickly reactivates to harmful levels even after years of treatment.

“Preserving and even increasing this defense in cells may make more HIV-infected persons into controllers and prevent HIV from rebounding to high and damaging levels when anti-HIV medications are stopped,” said Richard D’Aquila, M.D., the director of the Northwestern HIV Translational Research Center. He is the senior author of the study, which will be published Oct. 16 in the journal PLOS ONE.

D’Aquila also is the Howard Taylor Ricketts Professor of Medicine at Northwestern University Feinberg School of Medicine and a physician at Northwestern Memorial Hospital.

D’Aquila and colleagues now are working to develop a medicine that would boost this defensive immune protein called APOBEC3G, or A3 for short. 

The Missing Second Defensive Line

Much is known about how the immune system of controllers initially fights the virus. But HIV quickly escapes from that first line of defense by mutating and evading the adaptive immune system. How these individuals control HIV long term without medications to keep from developing AIDS has been under study by many researchers? It seemed there must be a second defensive line in the immune system.

Turning HIV Into a Wimp

In the new study, D’Aquila and his team have found that controllers, long after they have acquired HIV, have a more abundant supply of the critical immune protein A3 in specific white blood cells called resting memory T cells. This is where the virus lies silently in an inactive form and roars back when anti-retroviral drugs are stopped. In controllers, though, their bounty of A3 means that any new HIV made from those cells inherits a helping of A3, which turns the new viruses into harmless wimps that can’t infect other cells.

You Can’t Fool A3

The feisty A3 is a critical part of the newly characterized intrinsic immune system, and it resides in many cells of the immune system including resting T cells. Unlike the adaptive immune system, which fails to recognize the virus once it mutates its pieces, the intrinsic immune system can’t be fooled.

“The intrinsic immune system recognizes the basic guts of the virus — the nucleic acids — that HIV can’t change and then damages those nucleic acids,” D’Aquila said.

D’Aquila theorizes that the controllers’ first line of defense slows down the ability of HIV to destroy all the A3.

“Perhaps starting anti-HIV drugs very soon after HIV is caught, rather than the current practice of waiting until later to start, would work like the controllers’ first line of defense,” D’Aquila suggested. “If we preserve A3, it could minimize HIV’s spread through the body as this protein seems to do in controllers.”

Otherwise, D’Aquila theorizes, all reserves of the protein are wiped out if HIV replicates unchecked for several months.

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Countries with more wealth have higher Alzheimer’s risk

People living in wealthier countries with better access to clean water and good hygiene may have a higher risk of developing Alzheimer’s disease, Medical News Today reported.

In a study published in the journal Evolution, Medicine and Public Health, researchers analyzed data from the World Health Organization’s (WHO) Global Burden of Disease (GBD) report in 2009.

They noted that countries with better access to clean drinking water, lower rates of infectious disease and a greater percentage of the population residing in urban areas all had higher rates of Alzheimer’s disease, according to Medical News Today.

Researchers explained their findings using the ‘hygiene hypothesis,’ which suggests that people who live in places with access to better hygiene have less exposure to certain germs. With no harmful bacteria to fight, people’s immune system’s develop insufficiently, putting them at a higher risk for autoimmune diseases like dementia and Alzheimer’s.

“The ‘hygiene hypothesis,’ which suggests a relationship between cleaner environments and a higher risk of certain allergies and autoimmune diseases, is well-established,” lead study author Dr. Molly Fox, from the University of Cambridge, said. “We believe we can now add Alzheimer’s to this list of diseases.”

Currently, more than 50 percent of people with Alzheimer’s live in the developing world, and by 2025, this figure is expected to rise to more than 70 percent, according to Fox.

“An awareness of this by-product of increasing wealth and development could encourage the innovation of new strategies to protect vulnerable populations from Alzheimer’s,” Fox said.
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Migraines cause long-lasting changes to brain structure

Symptoms can include a pounding headache, nausea, vomiting and light sensitivity.

Migraine may have more impacts on your mind than you may have thought at first. Scientists have discovered that migraine could have long-lasting effects on the brain’s structure.

Traditionally, migraine has been considered a benign disorder without long-term consequences for the brain,” said Messoud Ashina, one of the researchers, in a news release. “Our review and meta-analysis study suggests that the disorder may permanently alter brain structure in multiple ways.”

Migraine affects about 10 to 15 percent of the general population and the impacts associated with migraine can cause a substantial personal, occupational and social burden. Symptoms can include a pounding headache, nausea, vomiting and light sensitivity. Because there are no official “cures” for migraine, this makes living with the condition difficult. That’s why it’s important to understand exactly what might cause migraine and what its effects might be on the brain.

In order to examine the impact of migraine, the researchers reviewed six population-based studies and 13 clinic-based studies. They examined whether people who experienced migraine or migraine with aura had an increased risk of brain lesions, silent abnormalities or brain volume changes on MRI brain scans in comparison to those without the conditions.

In the end, the researchers found that migraine with aura increased the risk of white matter brain lesions by 68 percent. Migraine with no aura, in contrast, increased the risk by 34 percent. The scientists also discovered that the risk for infarct-like abnormalities increased by 44 percent for those with migraine with aura compared to those without aura. In addition, brain volume changes were more common in people with migraine and migraine with aura than those with no migraines.

“We hope that through more study, we can clarify the association of brain structure changes to attack frequency and length of the disease,” said Ashina. “We also want to find out how these lesions may influence brain function.”

Currently the researchers plan to conduct further studies to investigate these lesions and migraine further.

The findings are published in the journal Neurology.