Actor Seth Rogen Shares a Heartbreaking Tale Before United States Senate Hearing on Alzheimer’s Research

Seth Rogen on Dementia at 55

On Wednesday, Seth Rogen gave impassioned testimony before a U.S. Senate subcommittee. The comedian and his wife Lauren Miller recently started a charity dedicated to Alzheimer’s education and research advocacy, Hilarity for Charity. Video of the ever-unassuming Rogen’s plea to support Alzheimer’s research resonated widely across the Internet, already having been viewed more than 3 million times on YouTube.

It’s not just that Rogen is a funny guy and that Alzheimer’s affects more than 5 million Americans, but also that a third of people fear dementia more than they do death. At odds with the massive public response to Rogen’s message, of the 18 members of the subcommittee, only two—Senators Tom Harkin and Jerry Moran—attended the hearing. “Not sure why only two senators were at the hearing,” Rogen tweeted. “Very symbolic of how the Government views Alzheimer’s. Seems to be a low priority.”

Read more.


What is Alzheimer’s disease? - Ivan Seah Yu Jun

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.



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.”


Seth Rogen Opening Statement on Alzheimer’s Disease. 

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 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:

Photo by AJ Cann Flickr user

From: Daily Anatomy

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.


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

Rescue of Alzheimer’s Memory Deficit Achieved by Reducing ‘Excessive Inhibition’

A new drug target to fight Alzheimer’s disease has been discovered by a research team led by Gong Chen, a Professor of Biology and the Verne M. Willaman Chair in Life Sciences at Penn State University. The discovery also has potential for development as a novel diagnostic tool for Alzheimer’s disease, which is the most common form of dementia and one for which no cure has yet been found. A scientific paper describing the discovery will be published in Nature Communications on 13 June 2014. 

Chen’s research was motivated by the recent failure in clinical trials of once-promising Alzheimer’s drugs being developed by large pharmaceutical companies. “Billions of dollars were invested in years of research leading up to the clinical trials of those Alzheimer’s drugs, but they failed the test after they unexpectedly worsened the patients’ symptoms,” Chen said. The research behind those drugs had targeted the long-recognized feature of Alzheimer’s brains: the sticky buildup of the amyloid protein known as plaques, which can cause neurons in the brain to die. “The research of our lab and others now has focused on finding new drug targets and on developing new approaches for diagnosing and treating Alzheimer’s disease,” Chen explained.

“We recently discovered an abnormally high concentration of one inhibitory neurotransmitter in the brains of deceased Alzheimer’s patients,” Chen said. He and his research team found the neurotransmitter, called GABA (gamma-aminobutyric acid), in deformed cells called “reactive astrocytes” in a structure in the core of the brain called the dentate gyrus. This structure is the gateway to hippocampus, an area of the brain that is critical for learning and memory.  

Chen’s team found that the GABA neurotransmitter was drastically increased in the deformed versions of the normally large, star-shaped “astrocyte” cells which, in a healthy individual, surround and support individual neurons in the brain. “Our research shows that the excessively high concentration of the GABA neurotransmitter in these reactive astrocytes is a novel biomarker that we hope can be targeted in further research as a tool for the diagnosis and treatment of Alzheimer’s disease,” Chen said. 

Chen’s team developed new analysis methods to evaluate neurotransmitter concentrations in the brains of normal and genetically modified mouse models for Alzheimer’s disease (AD mice). “Our studies of AD mice showed that the high concentration of the GABA neurotransmitter in the reactive astrocytes of the dentate gyrus correlates with the animals’ poor performance on tests of learning and memory,” Chen said. His lab also found that the high concentration of the GABA neurotransmitter in the reactive astrocytes is released through an astrocyte-specific GABA transporter, a novel drug target found in this study, to enhance GABA inhibition in the dentate gyrus. With too much inhibitory GABA neurotransmitter, the neurons in the dentate gyrus are not fired up like they normally would be when a healthy person is learning something new or remembering something already learned.

Importantly, Chen said, “After we inhibited the astrocytic GABA transporter to reduce GABA inhibition in the brains of the AD mice, we found that they showed better memory capability than the control AD mice. We are very excited and encouraged by this result because it might explain why previous clinical trials failed by targeting amyloid plaques alone. One possible explanation is that while amyloid plaques may be reduced by targeting amyloid proteins, the other downstream alterations triggered by amyloid deposits, such as the excessive GABA inhibition discovered in our study, cannot be corrected by targeting amyloid proteins alone. Our studies suggest that reducing the excessive GABA inhibition to the neurons in the brain’s dentate gyrus may lead to a novel therapy for Alzheimer’s disease. An ultimate successful therapy may be a cocktail of compounds acting on several drug targets simultaneously.”

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.

(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.

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.

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.

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:
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