alzhiemers

Yale School of Medicine researchers have discovered a protein that is the missing link in the complicated chain of events that lead to Alzheimer’s disease, they report in the September 4 issue of the journal Neuron. Researchers also found that blocking the protein with an existing drug can restore memory in mice with brain damage that mimics the disease.

“What is very exciting is that of all the links in this molecular chain, this is the protein that may be most easily targeted by drugs,” said Stephen Strittmatter, the Vincent Coates Professor of Neurology and senior author of the study. “This gives us strong hope that we can find a drug that will work to lessen the burden of Alzheimer’s.”

Scientists have already provided a partial molecular map of how Alzheimer’s disease destroys brain cells. In earlier work, Strittmatter’s lab showed that the amyloid-beta peptides, which are a hallmark of Alzheimer’s, couple with prion proteins on the surface of neurons. By an unknown process, the coupling activates a molecular messenger within the cell called Fyn.

In the Neuron paper, the Yale team reveals the missing link in the chain, a protein within the cell membrane called metabotropic glutamate receptor 5 or mGluR5. When the protein is blocked by a drug similar to one being developed for Fragile X syndrome, the deficits in memory, learning, and synapse density were restored in a mouse model of Alzheimer’s.

Strittmatter stressed that new drugs may have to be designed to precisely target the amyloid-prion disruption of mGluR5 in human cases of Alzheimer’s and said his lab is exploring new ways to achieve this.

http://scitechdaily.com/yale-scientists-discover-alzheimers-missing-link/

source 

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What an ‘Adamant’ Elderly Man Was Caught on Camera Doing With Two Cops Is Bound to Send the Video Viral

They didn’t have a choice.

Two police officers in Little Rock, Arkansas were left with only one option after finding a missing elderly man diagnosed with Alzheimer’s wandering the streets earlier this month — they had to help complete his mission.

Sgt. Brian Grigsby and officer Troy Dillard told the CBS Evening News that often deal with calls of Alzheimer’s patients wandering aimlessly, but Melvyn Amrine one was different.

According to the two officers, the “adamant” man was in a “moment of clarity” and simply out on a mission to purchase Mother’s Day flowers for his wife, as he had done every year since the birth of their first child — and he was not returning home until he had completed his task.

“He was pretty adamant,” Dillard told the CBS Evening News.

“He wasn’t going home until he got those flowers,” Grigsby added. “That’s what he wanted. He wanted flowers for his wife, because tomorrow was Mother’s Day.”

The officers had to help.

“We had to get those flowers,” Grigsby said. “We had to get them. I didn’t have a choice.”

So, after radioing dispatch and notifying them that Amrine had been found, they secretly took him to the grocery store.

Surveillance store footage captured the moments the officers assisted him select the bouquet, up until they loaned him some cash to pay for the flowers.

It was then time for him to surprise his wife of more than 60 years, Doris.

“As he came up those steps, and I saw those roses and the smile on his face, I just broke inside,” Doris told the CBS Evening News. “I just said, ‘Thank you, thank you.’ Because I saw his heart.”

She added that the act of love offered proof that “even though the mind doesn’t remember everything, the heart remembers.”

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Seth Rogen Opening Statement on Alzheimer’s Disease. 

npr.org
New Study Shows Brain Benefits Of Bilingualism

Being bilingual opens up new worlds to speakers. It also appears to delay the onset of dementia…

In the Hyderabad region, a language called Telugu is spoken by the majority Hindu group, and another called Dakkhini by the minority Muslim population. Hindi and English are also commonly spoken in formal contexts, including at school. Most people who grow up in the region, then, are bilingual, and routinely exposed to at least three languages.

The patients who contributed data to the study, then, are surrounded by multiple languages in everyday life, not primarily as a result of moving from one location to another. This turns out to be an important factor, as the authors explain:

In contrast to previous studies, the bilingual group was drawn from the same environment as the monolingual one and the results were therefore free from the confounding effects of immigration. The bilingual effect on age at dementia onset was shown independently of other potential confounding factors, such as education, sex, occupation, cardiovascular risk factors, and urban vs rural dwelling, of subjects with dementia.

In other words, thanks in large part to the study’s cultural context, these researchers made great progress zeroing in on bilingualism as the specific reason for the delay in dementia symptoms.

What exactly is it about the ability to speak in two languages that seems to provide this protective effect? Alladi and co-authors explain:

The constant need in a bilingual person to selectively activate one language and suppress the other is thought to lead to a better development of executive functions and attentional tasks with cognitive advantages being best documented in attentional control, inhibition, and conflict resolution.

Source: NPR.

Read the study in Neurology (behind a paywall). Or check out these open source links:

  • Delaying the onset of Alzheimer disease, Neurology 2010. 
  • Language Control in Different Contexts: The Behavioral Ecology of Bilingual Speakers, Frontiers in Psychology
  • A Longitudinal Study of Memory Advantages in Bilinguals, PLOS ONE.

Links via Nicodin Bogdan on Science in Google+.

A relatively young scientific method, optogenetics allows the manipulation of cell activity using light, enabling teams to control and monitor tissue in vivo even at the scale of complex organisms such as mice and other mammals.

Through this method, it is possible to apply changes to the behaviour of tissue and observe the effects in an organism at the speed of light. The method relies on genetically inserted channel proteins in the cell walls of optogenetic animals which are sensitive to specific frequencies of light. It is even possible, through insertion of the channel genes behind certain genetic ‘promoters,’ to isolate the expression of the channels to specific areas of the body such as a brain region so as to concentrate the effects on an area under study while preventing channels appearing elsewhere.

Thereafter, exposure to light can open or close these channels, allowing or preventing secretions of chemicals such as neurotransmitters; different effects can be obtained independently or simultaneously by using multiple frequencies of light from an implanted optrode (pictured above) and corresponding channels. The aforementioned device combines a laser emitter and electrode, which can simultaneously monitor neuron activity as well as administer pulses of laser light when needed.

What does all of this accomplish? Control to this extent allows research of living brains, the ways in which they function and the ways in which they fail to function. Right now, optogenetics is being applied to better our understanding of some of the most terrible neurological disorders such as Parkinson’s disease, Alzheimer’s and chronic anxiety. 

People with dementia are learning to live well with dementia, and one of the goals of Dementia Alliance International is to give a voice to, and to empower others with dementia, to live well to. We will publish articles on many of the issues we are facing, written by people with dementia, rather than by those without dementia, who choose to write or speak “about us, without us”.
— 

I repeat: “Please don’t call us sufferers”

tl;dr don’t use derogatory language (like “suffering”) to refer to people with dementia.

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Music and Memory Project


UCLA’s Easton Center is part of a nationwide program that accepts donations of old iPods and MP3 players to be used to help Alzheimer's  patients.

Patients with severe Alzheimer’s disease may respond to music, eliciting memories and socialization. Utilizing iPods and other MP3 players permits an individualized approach to music therapy for these patients through creation of playlists of music popular during their youth.

Read more about how to help with this project

A slice of a brain affected by Alzheimer’s disease

“The disease shrinks brain tissue and leads to severe memory loss. In this photo you can see the widened ventricles and shrinked grey matter.

Alzheimer’s is associated with a deficiency of the neurotransmitter acetylcholine. While there are no known cures for Alzheimer’s, there are some treatments available that can slow the condition down, and a promising array of new treatments on the horizon. Our increased understanding of biology and the human genetic code have many scientists hopeful for effective preventive measures and possibly even cures in the near future.”

Read more: http://alzheimersdaze.com/alzheimers/disease-characteristics/

Photo by AJ Cann Flickr user

From: Daily Anatomy

What is the difference between Alzheimer's disease and dementia?

“Dementia” is a term that has replaced a more out-of-date word, “senility,” to refer to cognitive changes with advanced age.

Dementia includes a group of symptoms, the most prominent of which is memory difficulty with additional problems in at least one other area of cognitive functioning, including language, attention, problem solving, spatial skills, judgment, planning, or organization. These cognitive problems are a noticeable change compared to the person’s cognitive functioning earlier in life and are severe enough to get in the way of normal daily living, such as social and occupational activities.

A good analogy to the term dementia is “fever.” Fever refers to an elevated temperature, indicating that a person is sick. But it does not give any information about what is causing the sickness. In the same way, dementia means that there is something wrong with a person’s brain, but it does not provide any information about what is causing the memory or cognitive difficulties. Dementia is not a disease; it is the clinical presentation or symptoms of a disease.

There are many possible causes of dementia. Some causes are reversible, such as certain thyroid conditions or vitamin deficiencies. If these underlying problems are identified and treated, then the dementia reverses and the person can return to normal functioning.

However, most causes of dementia are not reversible. Rather, they are degenerative diseases of the brain that get worse over time. The most common cause of dementia is AD, accounting for as many as 70-80% of all cases of dementia.

Approximately 5.3 million Americans currently live with AD. As people get older, the prevalence of AD increases, with approximately 50% of people age 85 and older having the disease.

It is important to note, however, that although AD is extremely common in later years of life, it is not part of normal aging. For that matter, dementia is not part of normal aging. If someone has dementia (due to whatever underlying cause), it represents an important problem in need of appropriate diagnosis and treatment by a well-trained healthcare provider who specializes in degenerative
diseases.

In a nutshell, dementia is a symptom, and AD is the cause of the symptom.

When someone is told they have dementia, it means that they have significant memory problems as well as other cognitive difficulties, and that these problems are severe enough to get in the way of daily living.

Most of the time, dementia is caused by the specific brain disease, AD. However, some uncommon degenerative causes of dementia include vascular dementia (also referred to as multi-infarct dementia), frontotemporal dementia, Lewy Body disease, and chronic traumatic encephalopathy.

Contrary to what some people may think, dementia is not a less severe problem, with AD being a more severe problem. There is not a continuum with dementia on one side and AD at the extreme. Rather, there can be early or mild stages of AD, which then progress to moderate and severe stages of the disease.

One reason for the confusion about dementia and AD is that it is not possible to diagnose AD with 100% accuracy while someone is alive. Rather, AD can only truly be diagnosed after death, upon autopsy when the brain tissue is carefully examined by a specialized doctor referred to as a neuropathologist.

During life, a patient can be diagnosed with “probable AD.” This term is used by doctors and researchers to indicate that, based on the person’s symptoms, the course of the symptoms, and the results of various tests, it is very likely that the person will show pathological features of AD when the brain tissue is examined following death.

In specialty memory clinics and research programs, such as the BU ADC, the accuracy of a probable AD diagnosis can be excellent. And with the results of exciting new research, such as that being conducted at the BU ADC, the accuracy of AD diagnosis during life is getting better and better.

This contribution was made by Dr. Robert Stern, Director of the BU ADC Clinical Core.

Source BU ADC Bulletin

Source: http://www.alzheimersreadingroom.com/2010/06/whats-difference-between-alzheimers-and.html

Lipid rafts participate in the renewal of brain neurons in Alzheimer’s disease

Research over decades has implicated aberrant autophagy and lysosomal function as reliable markers and therapeutic targets for neurodegenerative diseases. Lipid rafts are shown to participate in lysosomal reproduction, and some lysosomal storage diseases are proposed to result from the accumulation of lipids in late endosomal/lysosomal compartments. Prof. Lin Yuan and team from Southern Medical University in China review the influence of lipid rafts on the progression of Alzheimer’s disease through the modulation of aberrant autophagic-lysosomal pathway of amyloid-ß peptide, and bring forward a possible mechanism underlying the clearance of Alzheimer’s disease products, implicating the autophagic-lysosomal pathway from the perspective of “clearance” and “turnover” of cells. The relevant findings have been published in the Neural Regeneration Research (Vol. 9, No. 1, 2014).

Article: “ Lipid rafts participate in aberrant degradative autophagic-lysosomal pathway of amyloid-beta peptide in Alzheimer’s disease” by Xin Zhou, Chun Yang, Yufeng Liu, Peng Li, Huiying Yang, Jingxing Dai, Rongmei Qu, Lin Yuan (Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong Province, China)

Zhou X, Yang C, Liu YF, Li P, Yang HY, Dai JX, Qu RM, Yuan L. Lipid rafts participate in aberrant degradative autophagic-lysosomal pathway of amyloid-beta peptide in Alzheimer’s disease. Neural Regen Res. 2014;9(1):92-100.

Figure: Lipid rafts facilitate the production, aggregation, neuronal binding and toxicity of Aβ oligomers. (a) The Aβ peptide is produced by the lipid raft dependent sequential cleavage of APP, first by BACE1 and then by the γ-secretase complex; (b) Lipid raft components including cholesterol and sialic acid-containing gangliosides promote the aggregation of Aβ to form soluble oligomers; © Aβ oligomers bind to specific neuronal receptors within pathogenic lipid rafts, including PrPC and the NMDA and mGluR5 receptors. The resulting perturbations in neuronal function and survival underlie the memory impairments and cognitive decline which characterise Alzheimer’s disease.

cnn.com
Blood test predicts Alzheimer's disease

(CNN) – In a first-of-its-kind study, researchers have developed a blood test for Alzheimer’s disease that predicts with astonishing accuracy whether a healthy person will develop the disease.

Though much work still needs to be done, it is hoped the test will someday be available in doctors’ offices, since the only methods for predicting Alzheimer’s right now, such as PET scans and spinal taps, are expensive, impractical, often unreliable and sometimes risky.

“This is a potential game-changer,” said Dr. Howard Federoff, senior author of the report and a neurologist at Georgetown University Medical Center. “My level of enthusiasm is very high.”

The study was published in Nature Medicine.

‘We were surprised’

In the beginning, the researchers knew they wanted to find a blood test to detect Alzheimer’s but didn’t know what specifically to look for. Should they examine patients’ DNA? Their RNA? Or should they look for the byproducts of DNA and RNA, such as fats and proteins?

They decided to start with fats, since it was the easiest and least expensive. They drew blood from hundreds of healthy people over age 70 living near Rochester, New York, and Irvine, California. Five years later, 28 of the seniors had developed Alzheimer’s disease or the mild cognitive problems that usually precede it.

Scouring more than 100 fats, or lipids, for what might set this group apart, they found that these 28 seniors had low levels of 10 particular lipids, compared with healthy seniors.

To confirm their findings, the researchers then looked at the blood of 54 other patients who had Alzheimer’s or mild cognitive impairment. This group also had low levels of the lipids.

Overall, the blood test predicted who would get Alzheimer’s or mild cognitive impairment with over 90% accuracy.

“We were surprised,” said Mark Mapstone, a neuropsychologist at the University of Rochester Medical Center and lead author of the study. “But it turns out that it appears we were looking in the right place.”

Continue Reading.

Physicists push new Parkinson’s treatment toward clinical trials

Research at Michigan State University, published in the Journal of Biological Chemistry, shows that a small “molecular tweezer” keeps proteins from clumping, or aggregating, the first step of neurological disorders such as Parkinson’s disease, Alzheimer’s disease and Huntington’s disease.

S. Acharya, B. M. Safaie, P. Wongkongkathep, M. I. Ivanova, A. Attar, F.-G. Klarner, T. Schrader, J. A. Loo, G. Bitan, L. J. Lapidus. Molecular Basis for Preventing  -Synuclein Aggregation by a Molecular Tweezer. Journal of Biological Chemistry, 2014; 289 (15): 10727 DOI: 10.1074/jbc.M113.524520

A fullerene bound in a buckycatcher (molecular tweezer) through aromatic stacking interactions Reported by Sygula and coworkers.

Brain cells of a laboratory mouse glowing with multicolor fluorescent proteins. Image courtesy of Harvard University, Livett-Weissman-Sanes-Lichtman

Early growth factor treatment may help prevent cell loss in Alzheimer’s disease

Brain-derived neurotrophic factor or BDNF has long been a target of interest among Alzheimer’s disease (AD) researchers and the Alzheimer’s community at large.

Four years ago, Mark Tuszynski, MD, PhD, professor of neurosciences at UC San Diego School of Medicine and director of the Center for Neural Repair and colleagues showed that a BDNF-based treatment measurably improved neural dysfunction in animal models of Alzheimer’s disease. The findings garnered international headlines.

Now there is new evidence that BDNF may be effective as a preventive measure for AD. 

In a paper, published yesterday in The Journal of Neuroscience, Tuszynski and colleagues follow up with evidence that early life BDNF treatment prevents neuronal loss in mutant mice genetically predisposed to early-onset familial Alzheimer’s disease.

Specifically, mice engineered to express APP, a protein strongly linked to AD development, received injections of the BDNF gene at two months of age and were examined five months later. The researchers found that BDNF-treated mice exhibited better behavior and brain function than untreated APP mutant mice and suffered significantly less neuron loss in the entorhinal cortex, a region of the brain that helps mediate learning and memory.

In addition, they noted that BDNF did not affect amyloid plaque accumulation, another major indicator of AD, suggesting that direct amyloid reduction is not necessary to achieving significant neuroprotective benefits in mutant amyloid models of AD.

“These findings strengthen the rationale for planning human clinical trials of BDNF therapy in AD,” said Tuszynski. “This is an effort that we are actively engaged in.” 

Tuszynski also noted that there is a possibility that BDNF therapy and anti-amyloid therapies for AD could be combined to yield better treatments than either treatment alone.

This is my grandmother. She’s 85 (turning 86 in less than a month) and she’s an epic bad-ass who survived fleeing her homeland of Estonia by creating an acting troupe and hitching a lift across Europe until she found American soldiers. When the Americans came into town, everyone else hid because they were scared, but she put on her best (and only) frock and went out to wave hello. They gave her chocolate and new stockings.

She is the only person in my immediate family who has been to prison. One night, in Germany, her and her best girl-friend stayed out too late and got tipsy, breaking curfew, but only had to spend one night in jail because the police chief recognized her from a stage production of ‘Gaslight’. (She does not admit to this story.)

She is a troublemaker. Once, she went to the laundromat and accidentally tipped a whole box of detergent into an open machine and as the suds rose up and out, spilling over, she calmly picked up her clothing and walked out. (She does not admit to this story either, but will own up to, perhaps, paying for damages for something that she never did.)

She has Alzheimer’s and dementia. She knows who she is and where she is, but not when it is. There are days when the war is still going on. 

Today, she had a stroke. She’s fine, doing well, and all that good stuff, but as we were in the emergency room, the doctor came up to her and asked what she had for breakfast. Calm as can be, she deadpanned: “Two bottles of whisky and a fireman.”

From Neuroscience Research Techniques

Results from a new study in the Journal of Alzheimer’s Disease hints at a new potential cause for Alzheimer’s disease (AD): the accumulation of iron in brain cells. A key component of hemoglobin in the blood, iron rarely accumulates to toxic levels in the body. But scientists at #UCLAfound that the hippocampus–the center of memory and an area known to be affected early on in AD–had higher than expected amounts of iron in AD patients, and that hippocampal damage appeared to happen in tandem with increases in iron. The thalamus, which is largely spared until very late in AD, did not show these iron increases, nor did the brains of healthy patients. These results, the researchers say, may point to new potential AD treatments as well as environmental factors that may affect disease onset and progression.

Read more: http://bit.ly/19H93NU
Journal article: Increased Iron Levels and Decreased Tissue Integrity in Hippocampus of Alzheimer’s Disease Detected in vivo with Magnetic Resonance Imaging. Journal of Alzheimer’s Disease, 2013. doi: 10.3233/JAD-130209
Image credit: Wellcome Images