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BioWorld - Monday, March 2, 2026
Home » Authors » Anette Breindl

Anette Breindl

Articles

ARTICLES

Tau neuron illustration
Tautism?

Tau protein plays role in autism spectrum disorder

March 2, 2020
By Anette Breindl
Lowering levels of tau protein improved multiple symptoms of autism spectrum disorders (ASD) in two different mouse models of the disease, both of which are driven by hyperactivity of the mTOR PI3 kinase pathway.
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Virus research illustration

Bench Press for Feb. 28, 2020

Feb. 28, 2020
By Anette Breindl
BioWorld looks at translational medicine, including: Finding the next pandemic threat early on; Microglial fresh start helps heal brain trauma; Finding the silent majority; Anatomy study reveals schizophrenia subtypes; Increasing immune activity improves autoimmunity; How cancer cells hibernate…; …And who makes their bed; Blocking trash trashes MSI-hi tumors; New splicing factor implicated in muscular dystrophy.
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DNA sequencing

Passengers, noncoding genome affect how cancers play out

Feb. 28, 2020
By Anette Breindl
Beyond every binary is a more complex reality. And so it is with driver and passenger mutations. The separation of tumor mutations into drivers and passengers underpins much progress in the development of targeted therapies.
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BioWorld MedTech’s Diagnostics Extra for Feb. 27, 2020

Feb. 27, 2020
By Meg Bryant and Anette Breindl
Keeping you up to date on recent developments in diagnostics, including: Chest CT bests assays in diagnosing Covid-19; Sweat sensor keeps tabs on stress; Oligodendrocyte-neural connections not just about myelin; Sharper look yields new potential kinase target in ovarian cancer.
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Brain-DNA illustration

Trinucleotide expansions are too much of a good thing

Feb. 26, 2020
By Anette Breindl
Everything’s good for something. Including, it turns out, 5’ untranslated trinucleotide repeats. In the Feb. 17, 2020, issue of Nature Neuroscience, researchers have demonstrated a role for such repeats in controlling protein levels of fragile X mental retardation protein (FMRP).
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BioWorld MedTech’s Neurology Extra for Feb. 21, 2020

Feb. 21, 2020
By Andrea Applegate and Anette Breindl
Keeping you up to date on recent developments in neurology, including: Therapeutic cooling targets site of newborn brain injury; Boys with inattention-hyperactivity face increased risk for traumatic brain injuries; Nanogold improves MS symptoms; Thanks for the memories, myelin.
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SNHG12 knockdown

Bench Press for Feb. 21, 2020

Feb. 21, 2020
By Anette Breindl
BioWorld looks at translational medicine, including: Noncoding RNA protects blood vessel walls; PD-1 blockade interferes with opioid analgesia; T-cell population is biomarker for beta cell function; Glutaminase 1 is NASH target; Oligodendrocyte-neural connections not just about myelin; Sharper look yields new potential kinase target in ovarian cancer; Structural insights could enable specific activation of GPCRs; Autophagy activation may prevent metastasis; AI finds structurally unique antibiotics.
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BioWorld MedTech’s Diagnostics Extra for Feb. 20, 2020

Feb. 20, 2020
By Meg Bryant and Anette Breindl
Keeping you up to date on recent developments in diagnostics, including: Detailed mapping of breast tumors sheds light on role of genetic variations; Leveraging AI in breast cancer diagnosis; T cell population is biomarker for β-cell function; Oligodendrocyte-neural connections not just about myelin.
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DNA sequencing

Passengers, noncoding genome affect how cancers play out

Feb. 20, 2020
By Anette Breindl
Beyond every binary is a more complex reality. And so it is with driver and passenger mutations. The separation of tumor mutations into drivers and passengers underpins much progress in the development of targeted therapies. By looking at passenger mutations more carefully, though, researchers at Yale University have shown that passenger mutations, too, played a role in how tumors progressed.
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Progression of alpha-synuclein pathology
The lysosome link

Strengthening lysosomes could head Parkinson’s off at the pass

Feb. 19, 2020
By Anette Breindl
Parkinson’s disease (PD) is a neurodegenerative disorder. But not just. And it may not start that way. There is increasing evidence that a-synuclein, the protein whose aggregates eventually destroy midbrain dopaminergic neurons in PD (and that are the cause of other diseases collectively known as the synucleinopathies), first aggregates “in enteric neurons, the neurons that control gastrointestinal function,” Collin Challis told BioWorld.
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View All Articles by Anette Breindl

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