Health Observance

Alzheimer’s & Brain Awareness Month

ASBMB Today Staff
June 5, 2018

Each year in June, the Alzheimer’s Association organizes Alzheimer’s & Brain Awareness Month to rally behind those with the devastating neurodegenerative disease. The ASBMB participated in the observance by sharing stories and studies of interest to patients, caregivers and researchers.

Thematic review series: ApoE and lipid homeostasis in Alzheimer’s disease
Alzheimer’s disease is the chief cause of dementia in adults in the U.S., accounting for up to 80 percent of all cases. While it is commonly known that age is the biggest risk factor of Alzheimer’s, the next major risk factor is less well known: a protein called apolipoprotein E, or ApoE. These eight review articles, published in 2017 in the Journal of Lipid Research, explore the connections between brain lipids, ApoE and Alzheimer’s. Learn more about the series.Read the reviews.

Virtual issue: Amyloids, prions and protein oligomers
Protein aggregation into amyloid oligomers and fibrils plays a key role in a wide range of diseases as well as normal biological function. The Journal of Biological Chemistry assembled a collection of research papers published in the past few years about amyloid structure, aggregation pathways and cell-to-cell propagation. See the virtual issue.

Feature: The quiet creep of Alzheimer’s disease
As caregivers grapple with the grim changes in their loved ones, researchers race to stall this neurodegenerative disorder. Read our ASBMB Today feature story from 2013.

Thematic review series: The molecular basis of Alzheimer’s disease
In one of its very first thematic review series, back in 2008, the Journal of Biological Chemistry zeroed in on the pathobiology of Alzheimer’s. Organized by then-Associate Editor Kenneth Neet of the Chicago Medical School at Rosalind Franklin University of Medicine and Science, who passed away this year, the series covered in a dozen articles the formation of amyloid oligomers; the fibrillization, degradation, and neurotoxicity of amyloid beta; Tau mutations in Alzheimer’s-like diseases; the association of ApoE with the disease; and mouse models for Alzheimer’s. Read the reviews.

Q&A with Paul Fraser, researcher of sporadic and familial Alzheimer’s disease
University of Toronto professor Paul Fraser has been an associate editor for the Journal of Biological Chemistry since 2011. Before that, he served as an editorial board member for more than eight years. An expert in neurodegenerative diseases, Fraser focuses on the biochemistry and biophysics of amyloid plaques and their connections to Alzheimer’s disease. Read the Q&A.

Thematic review series: Prions and prion-like proteins
More than 30 years ago, Stanley Prusiner at the University of California, San Francisco, coined the term “prion” and began to develop evidence to support his radical hypothesis for a new kind of infectious agent. Since then, the prion hypothesis – that scrapie, a fatal neurodegenerative disease in sheep and goats, is caused by a misfolded protein devoid of a genomic component – has been proved. The new dogma that resulted has been fruitful for guiding new approaches to studying Alzheimer’s and Parkinson’s diseases. In addition, emerging biochemical details of the pathogenesis of misfolded proteins are beginning to provide potential targets for therapy. In a thematic minireview series in the Journal of Biological Chemistry, Prusiner and other researchers cover prion replication, transmission and neurotoxicity. Learn more about the series.Read the reviews.

Essay: My spouse and the mouse
In ASBMB Today’s “Derailed But Undeterred” essay series, Harvey J. Armbrecht writes: “In my wife, it began at age 58 with pronouns. Linda began referring to our female pets as ‘he.’ No big deal. We joked about it. But gradually more serious symptoms appeared — short-term memory loss, the inability to concentrate, confusion in social situations and finally hallucinations. She ultimately was diagnosed with Lewy body disease, a relative of Alzheimer’s disease with no cure.” Read Armbrecht’s piece.

Profile of Virginia M-Y Lee
Virginia Lee is director of the Center for Neurodegenerative Disease Research at the University of Pennsylvania. She studies proteins involved in Alzheimer’s, Parkinson’s, frontotemporal dementia and amyotrophic lateral sclerosis, known as ALS or Lou Gehrig’s disease. In 1991, a team led by Lee and her husband, John Trojanowski, demonstrated that tau is a building block of neurofibrillary tangles in Alzheimer’s. Learn more about her career path and research.

Mouse lemurs and the brain
When kept in labs, mouse lemurs develop Alzheimer’s-like brain plaques at three to four years old. But out in the rainforests of Madagascar, the mammalian model organisms have been found to live well past a decade without exhibiting any signs of neurodegeneration. Learn more about this fascinating animal model.

Minireview: Astrocytic glycogen metabolism in the healthy and diseased brain
There is abundant evidence for a key role of glycogen in brain function. A recent Journal of Biological Chemistry minireview covers the physiological brain functions that depend on glycogen, discusses glycogen metabolism in disease, and investigates how glycogen breakdown is regulated at the cellular and molecular levels. Read the minireview.Read the entire thematic series on brain glycogen metabolism.

Tabor award winner Richard Karpowicz
One key question about both Alzheimer’s disease and Parkinson’s is how aggregation that starts in one cell is able to spread to others. Richard Karpowicz, a 2017 Herbert Tabor Young Investigator Award recipient, developed a fluorescent tagging strategy to monitor aggregated proteins as they enter the cell. Read about the work here. Read about what motivated Karpowicz to study the problem in this profile.

Feature: Puzzling out Parkinson's
Much like Alzheimer’s disease, Parkinson’s stems from the aggregation of a misfolded protein. In Parkinson’s, that protein is alpha-synuclein. New research focuses on disrupting this process by figuring out how molecules lurking in the gut microbiome end up affecting the brain. Read the cover story of the April issue of ASBMB Today.

Research paper: Annexin–tau interaction
As neurons form, the protein tau becomes enriched in the axon, where it remains concentrated in the healthy brain. In Alzheimer's disease, however, tau moves from the axon to the somatodendritic compartment, where it aggregates into fibrils. How this redistribution happens is not well understood. But a research team reported new insights in the Journal of Biological Chemistry in April. Read the paper.

Research paper: Extracellular alpha-synuclein S1P1 receptor out of lipid rafts
In order for diseases like Lewy body dementia and Parkinson’s disease to progress, it’s thought that alpha-synuclein must spread from cell to cell. However, how alpha-synuclein behaves while it’s outside of cells is poorly understood. Researchers reported in the Journal of Biological Chemistry that extracellular alpha-synuclein causes a particular receptor to be expelled from lipid rafts in cell membranes, disrupting a G-protein signaling process involved in cargo sorting and trafficking in the cell’s vesicles. While it’s still unknown whether this process contributes to pathology, this study shows that alpha-synuclein might have unexpected effects in different contexts. Read the paper.

Research paper: A function for the protease BACE1 in modulating the neuronal surface proteome
The protease BACE1 cleaves the amyloid precursor protein into amyloid-𝜷 peptides, which aggregate in the brain of Alzheimer’s patients. A variety of drugs to inhibit BACE1 have been tested or are in clinical trials. In a recent article in the journal Molecular & Cellular Proteomics, researchers used a targeted glycoproteomics method to show that BACE1 inhibition increases the abundance of unprocessed amyloid precursor protein but also increases the level of other substrates and even nonsubstrate proteins, suggesting that drugs to inhibit BACE1 may have unexpected side effects. Find out more in the article.

Research paper: Ceramide regulates mitochondrial ATP release
Amyloid-beta peptide activates an enzyme that releases a lipid called ceramide from the plasma membrane. Higher ceramide is associated with cell death. In the Journal of Lipid Research, scientists report that ceramide can block the voltage-dependent anion channel in the mitochondria, which alters the amount of ATP that can pass from the mitochondria into the cell at large. The researchers suggest that preventing synthesis of ceramide may protect mitochondria from damage inflicted by amyloid beta. Read the article here.

Review article: What can proteomics tell us about the Alzheimer’s brain?
A 2015 review in the journal Molecular & Cellular Proteomics covered how proteomic studies had helped understand Alzheimer’s disease. The authors focused on how proteomics can help find biomarkers that might be useful in diagnosing the disease or monitoring its progression, especially as new therapies are tested. Read more here.

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