Using torpedo-like, modified DNA snippets to blast mRNAs out of the cell, scientists lowered the amount of ataxin-2 protein. This allayed disease in mouse models of two neurodegenerative disorders.
The microbial communities teeming in the intestine of people recently diagnosed with PD differed markedly from those of healthy controls.
Three anti-tau antibodies are in Phase 1 or 2, while the first O-GlcNAcase inhibitor got the green light to start testing.
Manufacturers of a therapy system called neuroAD, which combines transcranial magnetic stimulation with cognitive training, are applying for FDA marketing clearance.
Overexpressing miR-132 dampened AD pathology in young mice, and appeared to nourish the birth of new hippocampal neurons in older animals.
As the brain ages, what protects it from cognitive decline? A two-day conference focused on reserve and resilience.
Showcasing forays into the biology of tau, researchers at AD/PD reported news on tau’s transcriptional regulation, its bungling of synaptic vesicles, its sway over the epigenome, and even flashed an atomic structure.
Need another reason to grab water instead of a soda? Beverages with added sugar—natural or artificial—are linked to smaller brain volume, worse memory, and tripled odds of stroke and dementia.
For years, many scientists considered transcranial magnetic stimulation to be a soft science on the fringes of drug development. After all, who could know exactly what a neural stimulation delivered from outside the head would do to the brain? Alas, TMS has become respectable for depression and migraine, complete with FDA approval, consensus guidelines, and routine administration. Now the TMS field is reaching for a win in Alzheimer’s disease, too. At the 13th AD/PD conference held recently in Vienna, researchers claimed not only that a phase 3 trial met the primary endpoint, but that they are awaiting FDA approval before too long. What’s the data? Madolyn Rogers reports.
Alzforum is pleased to release Version 2.0 of the AlzBiomarker database. This resource organizes decades of data on CSF and blood markers and provides a bird’s-eye view of the AD biomarker landscape. AlzBiomarker 2.0 adds findings from 43 additional studies published through May 2016. Besides updating 19 existing meta-analyses, we created two new ones, assessing whether CSF Aβ38 and YKL-40 correlate with cognitive decline. All analyses are displayed as interactive plots for easy exploration of the underlying data.
If you missed last week’s Alzforum webinar, you can now view the slides and listen to the conversation at your leisure. Asa Abeliovich and Hervé Rhinn discussed their recent Cell Systems paper with Rosa Rademakers, Jernej Ule, and Tony Wyss-Coray. Their topic was Δ-aging. This unbiased approach identifies why a person’s brain seems to be aging unusually fast or slowly by comparing their age-related cortical gene expression to normative rates of change in their peers. A genome-wide association study against this Δ-aging measure turned up none other than the frontotemporal dementia gene progranulin and its expression regulator, TMEM106B. A new approach to find genes and pathways of aging?
For a single protein, tau sure gives researchers a lot to talk about. This was obvious at the AD/PD meeting, where scientists presented all manner of findings about a microtubule binding protein that stokes neurodegeneration. A 3.4A structure of tau fibrils from the human brain wowed the audience, tau aggregates were found to cover synaptic vesicles like a wet blanket, an lncRNA was fingered in tau’s translational regulation, and tau pathology appeared to stamp the epigenome of the human brain. Read Alzforum’s latest AD/PD story for summaries of these and other selected tau findings from the meeting.
- Mony de Leon, Yi Li and Henry Rusinek on Next-Generation Tau PET Tracers Strut Their Stuff
- Agneta Nordberg on Next-Generation Tau PET Tracers Strut Their Stuff
- Ming-Kuei Jang on Next-Generation Tau PET Tracers Strut Their Stuff
- Einar Sigurdsson on Nice Catch? Antibodies Stabilize Tau in the Blood; Mark Levels in Brain
- Steve Barger on From Garbage Disposal to Neuromodulation? Membrane Proteasomes Churn Out Stimulating Peptides
- Lennart Mucke on Childhood Epilepsy Begets Adult Amyloid
- Jeffrey L. Noebels on Childhood Epilepsy Begets Adult Amyloid
- Niklas Mattsson, Henrik Zetterberg, Kaj Blennow and Ulf Andréasson on Blood Neurofilament Light a Promising Biomarker for Alzheimer’s?
- Paul Aisen on Blood Neurofilament Light a Promising Biomarker for Alzheimer’s?
- Marc Suárez-Calvet and Christian Haass on Can Immune Gene Expression Predict Pace of Motor Neuron Destruction?
- Markus Otto on Can Immune Gene Expression Predict Pace of Motor Neuron Destruction?
- Johnathan Cooper-Knock on Can Immune Gene Expression Predict Pace of Motor Neuron Destruction?
- Laura Piccio on Can Immune Gene Expression Predict Pace of Motor Neuron Destruction?
- David Corey on Poly Dipeptide in Cerebrospinal Fluid Marks C9ORF72 Expansion Carriers
- Dieter Edbauer on Poly Dipeptide in Cerebrospinal Fluid Marks C9ORF72 Expansion Carriers
- Michal Schwartz on Can Immune Gene Expression Predict Pace of Motor Neuron Destruction?
- Marcia Ratner on In Cognitively Normal Men, Antioxidants Fail to Reduce Dementia Risk
- Rahul Desikan on Genetic Risk Score Combines AD GWAS Hits, Predicts Onset
- Lawrence Rajendran on Infrared Microscopy Reveals Pre-Plaque Formation of β-Sheets by Aβ
- John Cirrito on From Garbage Disposal to Neuromodulation? Membrane Proteasomes Churn Out Stimulating Peptides
- Patrick Fraering on Tetraspanin 6: a pivotal protein of the multiple vesicular body determining exosome release and lysosomal degradation of amyloid precursor protein fragments.