Does a Breached Blood-Brain Barrier Cause Seizures in AD?
Researchers link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
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Janus-Faced PLCγ2? Alzheimer’s Risk Protein Toggles TREM2 and TLR Pathways
Acting downstream of TREM2, PLCγ2 facilitates phagocytic microglial behavior such as lipid processing. PLCγ2 also acts downstream of toll-like receptors, where it can throw a switch to inflammation.
Tau: Why Alzheimer’s Worsens Fast in Some, Slowly in Others
A postmortem study found that people who had more aggregation-prone, hyperphosphorylated, oligomeric forms of tau in their brains also had a more aggressive form of Alzheimer’s disease during life. Will we personalize tauopathy care like cancer care?
Does a Stimulating Childhood Stem Amyloid Plaques in Golden Years?
Cognitive enrichment in early life correlated with less Alzheimer’s pathology, and slower cognitive decline, in late life.
Doubling Rab5 in Mice Leads to Neurodegeneration—Without Plaques
Overexpressing the endosomal activator in neurons not only caused those organelles to swell, but also bungled synaptic transmission, goaded hyperphosphorylation of tau, and destroyed cholinergic neurons.
Algorithm Bests Humans in Predicting Alzheimer’s
A person's blood phospho-tau level, combined with his or her APOE genotype and scores on executive function and memory tests, outperforms the clinician in predicting dementia within the next four years.
Aducanumab Approval Sparks Backlash
Industry analysts and watchdogs have heaped criticism on the FDA, while Alzheimer’s researchers remain divided over whether the decision helps or harms the field.
With Little Data to Go On, Clinicians Are Left To Figure Out Way Forward
Trial data for aducanumab did not answer key questions, such as how long patients should stay on drug, leaving clinicians around the world to struggle with practical and ethical issues.
Double Whammy: APP Uppsala Deletion Ups Aβ and Its Aggregation Propensity
Found in one Swedish family, this mutation speeds up plaque deposition by way of two different mechanisms, leading to disease onset as young as age 40.
Can a Single Amyloid PET Scan Predict Time to Symptom Onset?
Amyloid Time: Because amyloid burden grows at a constant rate after having crossed a tipping point, scientists were able to predict when a person’s symptoms will begin, using only his or her age and one PET scan.
Intruder Alert: Inflammatory T Cells Lurk Near Lewy Bodies, Neurons
In Lewy body dementia brain tissue, CD4+ T cells loitered near synuclein aggregates and dopaminergic neurons. In vitro, T cells reacted to α-synuclein fragments by spewing the pro-inflammatory cytokine interleukin 17A.
Aβ Clearance—The Untapped Potential of Astrocytes?
A combination of retinoic acid and the cholesterol drug gemfibrozil prompted astrocytes to ingest and degrade Aβ. Mice treated this way had fewer amyloid plaques and performed better on cognitive tests.
On Aduhelm, Medicare Agency Gets Pressure From All Sides
The comment period ends with nearly 10,000 submissions split between pro and con, letter-writing campaigns, and scrutiny from U.S. Congress. Even so, scientists say, not much has changed.
Healthy, Drug-Resistant Microglia Reinvigorate Mouse Brain
Courtesy of one changed amino acid, human microglia resist drugs that typically destroy them. The cells behave normally and replenish endogenous mouse microglia
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?
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