Interactions with both remote and local amyloid-laden neurons drive tangles through the Alzheimer's brain. Is person-to-person variability in these interactions why patients differ in their progression?
In its national coverage determination, Medicare limits Aduhelm coverage to clinical trials, but OKs registry-based studies for traditionally approved anti-Aβ antibodies. This may change once new efficacy data comes out.
Low levels of Aβ37, 38, 40 reflect low processive activity of γ-secretase. They track with age at onset in people with autosomal-dominant mutations, and may track with cognitive decline in sporadic AD.
Applied to more than 500 alleles in APP, PSEN1, and PSEN2, the new classification can help scientists gauge how pathogenic, or benign, a given variant might be
In a game changer for the field, three papers report similar structures for TMEM106b fibrils. One claims they comprise the lion’s share of TDP-43 aggregates.
In the field's quest for disease-modifying treatments, two different α-synuclein vaccines and two antibodies look promising in preclinical studies, as well.
New, unbiased single-cell methods uncover coordinated changes in cell populations and their interactions. These correlate with disease pathology, progression.
DOPEGAL is produced in the locus coeruleus, the initial site of tau aggregation. In tauopathy mice, suppressing DOPEGAL prevented the spread of pathological tau.
By triggering release of mitochondrial DNA, tau fibrils may set off a cytosolic sensor that activates the interferon response. Blocking this sensor spared neurons and memory in mice.
At AD/PD, some speakers sought to bolster the argument that amyloid removal slows cognitive decline, while others identified what type of patient is most likely to benefit.