Side Effects of Alzheimer's Gene Visible in Child Brain Development

Certain genes increase the risk of developing Alzheimer's disease. The side effects of the most common of these genes, apolipoprotein E, may be evident as early as in childhood, a study finds.

Genetic risks are just one of the factors that may increase or decrease a person's chances of developing Alzheimer's disease (AD), along with age and family history.

While the symptoms of the rarer early-onset AD - representing less than 5 percent of people with the disease - can appear from the age of 30, the symptoms of the more common type, late-onset AD, is apparent over the age of 65.

This study, published in the online issue of Neurology, finds that the effects of the AD gene apolipoprotein E (APOE) may possibly be seen before the age of 20.

Read more: Side Effects of Alzheimer's Gene Visible in Child Brain Development

Studying genes in childhood that increase the risk of developing Alzheimer's disease may possibly
help experts develop ways of delaying the disease.

Source: medicalnewstoday

Dopamine Neuron Discovery Might Revolutionize Parkinson’s Treatments

Northwestern University researchers say they have identified the neurochemical signal likely missing in Parkinson’s disease. They reportedly discovered two distinctly different kinds of neurons that deliver dopamine to an important brain region responsible for both movement and learning/reward behavior.

“It has been dogma for decades that all dopamine neurons are somehow involved in both movement and reward, but this didn’t really make sense,” said Daniel A. Dombeck, Ph.D., the study’s senior author. “Now, it is so obvious in our recordings that there are different kinds of neurons. We can literally see this in behaving animals. Our findings will likely help answer many questions about Parkinson’s disease and other neurological mysteries.”

Read more: Dopamine Neuron Discovery Might Revolutionize Parkinson’s Treatments

Source: genengnews

The Pathophysiology of Defective Proteostasis in the Hypothalamus — From Obesity to Ageing

Hypothalamic dysfunction has emerged as an important mechanism involved in the development of obesity and its comorbidities, as well as in the process of ageing and age-related diseases, such as type 2 diabetes mellitus, hypertension and Alzheimer disease. In both obesity and ageing, inflammatory signalling is thought to coordinate many of the cellular events that lead to hypothalamic neuronal dysfunction. This process is triggered by the activation of signalling via the toll-like receptor 4 pathway and endoplasmic reticulum stress, which in turn results in intracellular inflammatory signalling. However, the process that connects inflammation with neuronal dysfunction is complex and includes several regulatory mechanisms that ultimately control the homeostasis of intracellular proteins and organelles (also known as 'proteostasis'). This Review discusses the evidence for the key role of proteostasis in the control of hypothalamic neurons and the involvement of this process in regulating whole-body energy homeostasis and lifespan.

Key points

• Specialized neurons of the hypothalamus control caloric intake and energy expenditure in response to hormonal, nutritional and neural signals that reflect the energy stores in the body
• Malfunction of the hypothalamus occurs in obesity and ageing, which leads to an imbalance between caloric intake and energy expenditure resulting in positive energy balance and reduced lifespan
• The excessive consumption of certain nutrients and ageing affect different aspects of proteostasis in selected neurons of the hypothalamus, contributing to neuronal dysfunction in obesity and ageing
• Inflammation is one of the most important outcomes of disturbed proteostasis to occur in the hypothalamus during obesity and ageing
• Several genetic and pharmacological approaches used to correct the defects of proteostasis and reduce inflammation have proven effective in reducing obesity and increasing lifespan in experimental models

Read more: The Pathophysiology of Defective Proteostasis in the Hypothalamus — From Obesity to Ageing

Figure 1: Control of energy balance and lifespan by the hypothalamic network. Neurons of the
medium hypothalamus respond to systemic signals of whole-body energy status. Blood levels of
insulin fluctuate acutely in response to carbohydrates present in food and chronically in response
to increased adiposity.

Source: Nature Reviews Endocrinology

Scientists Offer New View on Origins of Parkinson's Disease

The death of brain cells in Parkinson's disease is likely a result of stress in their endoplasmic reticulum or protein-folding machinery rather than just a general failure of their mitochondria or powerhouses.

So conclude researchers from the University of Leicester in the United Kingdom, who report their findings, based on research conducted in fruit flies, in the journal Cell Death and Disease.

Dr. Miguel Martins, who heads a group in the MRC Toxicology Unit at Leicester, says:

"This research challenges the current held belief the Parkinson's disease is a result of malfunctioning mitochondria."

Read more: Scientists Offer New View on Origins of Parkinson's Disease

Source: medicalnewstoday

Neurodegenerative disease damage reversed in fruit flies

Alzheimer's and Parkinson's symptoms have been reversed in fruit flies following treatment with a drug-like chemical, says research published in the Proceedings of the National Academy of Sciences.

The discovery, which centers around the protection of brain cells, could be a turning point in the fight against neurodegenerative disease, say the authors.

Neurodegenerative diseases occur when groups of nerve cells in the brain die, making it difficult for a person to move and to think.

According to Claire Bale, of Parkinson's UK, the symptoms of Parkinson's tend not to appear until 70 percent of nerve cells in the brain have already been lost.

Unfortunately, current treatments are only able to tackle the symptoms of the condition - they cannot slow or stop the degeneration of these cells.

Read more: Neurodegenerative disease damage reversed in fruit flies

Scientists are making progressing in techniques to protect nerve cells.

Source: medicalnewstoday

Organ regeneration with skin cells turning Into brain and heart cells

In a breakthrough study, researchers were able to chemically change skin cells to heart and brain cells.

When a person’s own body fails them, there are plenty of roadblocks to getting it running again. Adult hearts have a very limited ability to regenerate, so oftentimes the only way to help a person with a failing heart is to get them a new one. This is risky, though, since the patient’s body may reject even a perfectly matched organ. Scientists have been making strides in overcoming that problem by using a patient’s own stem cells to regenerate tissue, and researchers from the Gladstone Institutes have made a major breakthrough in the area — they successfully used a combination of chemicals to transform skin cells into heart and brain cells.

The feat is unprecedented, since all previous attempts to reprogram cells required scientists to add outside genes. Published in Science and Stem Cell, the research gives scientists a foundation for one day being able to regenerate lost or damaged cells with pharmaceuticals. The system is both more reliable and efficient than previous processes, and avoids medical concerns surrounding genetic engineering.

“This method brings us closer to being able to generate new cells at the site of injury in patients,” Dr. Sheng Ding, a Gladstone senior investigator, said in a press release. “Our hope is to one day treat diseases like heart failure or Parkinson’s disease with drugs that help the heart and brain regenerate damaged areas from their own existing tissue cells. This process is much closer to the natural regeneration that happens in animals like newts and salamanders, which has long fascinated us.”

Read more: Organ regeneration with skin cells turning Into brain and heart cells 

Brain cells are hard to fake, but it may now be possible.

Source: Pixabay