11170 RESULTS
COMMENT This paper reported very interesting findings that higher CSF GAP43 levels were associated with faster Aβ-related tau accumulation and spreading to connectivity-associated regions. This suggests a clear relation of the presynaptic protein to amyloid (A) a
COMMENT Immunization with fAβ42 (AN1792) results in a nearly complete absence of Aβ plaque deposits, both in mice that were vaccinated prior to the onset of amyloid deposition and in animals that were vaccinated after amyloid deposition was well underway. However
COMMENT Cancelling Aduhelm is an uncontroversial decision. Aducanemab was the vehicle on which FDA established its approval standards for amyloid antibodies: (1) plaque lowering buys accelerated approval, and (2) a touch of statistical significance on a composite
COMMENT This paper is impressive. It stands to become the pivotal reference work for the posterior cortical atrophy syndrome. It also reminds us that the mapping of syndrome to neuropathology is probabilistic rather than deterministic (Mesulam and Weintraub, 1992
COMMENT This work is by far the largest study of PCA to date. It solidifies evidence from many smaller studies that PCA is a distinct syndrome, usually causes young-onset dementia, mean age at onset about 60 years, and is almost always underpinned by Alzheimer’s
COMMENT As we explore the pathobiology of ApoE in AD and related dementias, there is an urgent need to understand the biochemical and biophysical properties of ApoE with the three main isoforms, ApoE2, ApoE3, and ApoE4 having differential effects on amyloids, cer
COMMENT This study uses antibody labeling and cryogenic electron microscopy to propose a model of lipidated apoE, the major functional form of this important apolipoprotein. Currently we have atomic structures of lipid-free, full-length modified human apoE and it
COMMENT As far as I know, this is the first evidence supporting that Alzheimer’s (and not just CAA) is transmissible in humans. If Alzheimer’s were to be transmissible, that would certainly open up a range of questions and concerns, including whether other, more
COMMENT The Collinge group has performed a measured, thoughtful, and careful report of dementia following iatrogenic exposure of people to pituitary extracts that contained Aβ seeding activity. The story is compelling to the extent that the group of patients were
COMMENT If self-replicating protein aggregates are the trigger for Alzheimer's disease, then the disease must in principle be transmissible. It is as simple as that. After the transmissibility of the pathology has been demonstrated in animals and humans, the
COMMENT Iatrogenic Alzheimer’s disease: a medical misadventure? Premised on our current understanding of the continuum of pathogenic changes in AD evolution, the U.K. National Prion Monitoring Cohort (NPMC) now reports eight cases of likely young-onset (38-55 yea
COMMENT The study is extremely interesting on the hot topic of potential transmission of Aβ in similar fashion as prion protein. The advent of acquired “mad cow” disease led to new standards of instrument handling when CJD is suspected. This has arguably led to s
COMMENT This very interesting paper is, as far as I know, the first demonstration of potential iatrogenic AD; previous cases had pointed to iatrogenic CAA. As cases are extremely rare, I think more research is warranted. The findings are not entirely surprising g
COMMENT This carefully considered, well-argued analysis of a small case series strongly suggests that iatrogenic transmission of Aβ in the course of human cadaver-derived pituitary growth hormone replacement therapy can induce not only CAA and diffuse Aβ plaques
COMMENT This is a very thorough report on a group of patients who received human cadaveric pituitary-derived growth hormone containing Aβ seeds in childhood for variable conditions and developed early onset of dementia with AD-like features in their 40s and 50s.
