Brain Endothelial Cells Are Diverse, Perturbed by Amyloid
Single-nucleus RNA-Seq of human brain finds regional differences in endothelial cell subtypes. Transcriptomes change in the presence of plaque or vascular amyloid.
NEWS
Take a Deep Breath—It Just Might Lower Your Risk for Alzheimer’s
Volunteers who practiced daily slow-breathing exercises for a month lowered Aβ42 in their blood; could this diminish the risk of AD?
Masking a Splicing Site Compensates for TDP-43 Dysfunction
Antisense oligonucleotides prevent mis-splicing of stathmin-2 when TDP-43 abandons the nucleus in human induced motor neurons or in the mouse brain.
Exosomes From Living Mice Hint That Sexes Respond Differently to Amyloid
The protein content of extracellular vesicles sampled from hippocampal interstitial fluid depended on age, sex, and amyloid load.
Phospho-tau/tau Ratios: Better Markers than Absolute p-Tau Levels?
The p-tau217/tau217 ratio in the cerebrospinal fluid tightly correlated with amyloid, while p-tau205/tau205 best detected neurofibrillary tangles and neurodegeneration.
Neurodegeneration—It’s Not the Tangles, It’s the T Cells
Summoned by microglia, T cells trigger neurodegeneration in a mouse model of tauopathy. Does this happen in Alzheimer’s disease?
Legacy of A4 Secondary Prevention Study Goes Beyond Negative Result
The decade-long trial found no benefit for solanezumab in delaying progression, but laid the groundwork for subsequent prevention studies.
Could Calming Overactive Ryanodine Receptor Restore Autophagy?
These endoplasmic reticulum channels can flood the cytosol with calcium, disrupting lysosomal acidification and stalling autophagy.
SPOTLIGHT
Take a Deep Breath—It Just Might Lower Your Risk for AD
Could changing your breathing help prevent Alzheimer’s disease? A provocative new study hints it might. Healthy adults who practiced a biofeedback-guided slow-breathing exercise for a month lowered the amount of Aβ42 and Aβ40 in their blood. As one of the first behavioral interventions to move Aβ in the desired direction, scientists said the approach deserves more study.
Masking Splicing Sites Compensates for TDP-43
In TDP-43 proteinopathies, the RNA/DNA binding protein leaves its post in the nucleus, allowing transcript mis-splicing to run amok. Now, researchers report that they can correct mis-splicing of STMN2, a protein essential for survival of neurons, without even touching TDP-43. Antisense oligonucleotides against a cryptic splice site in STMN2 prevent splicesomes from incorporating a cryptic exon in human motor neurons and mice with STMN2.
Are P-tau/tau Ratios the Best ATN Markers?
Evidence continues to build for using phospho-tau species in the cerebrospinal fluid or blood to detect amyloid plaques, neurofibrillary tangles, and even neurodegeneration. The latest suggests that the certain p-tau/tau ratios detect pathology better than do absolute p-tau concentrations. CSF p-tau217/tau217 correlate tightly with amyloid PET, even outdoing the Aβ42/40 ratio. CSF p-tau205/tau205, on the other hand, correlated poorly with plaques but very well with tau PET, and with regional brain atrophy, making it a potential marker for tangles and neurodegeneration.
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