In collaboration with the Banner Alzheimer’s Institute, Eli Lilly will test the anti-amyloid immunotherapy in cognitively normal people with a high risk for AD based on plasma phospho-tau-217.
A subset of cognitively normal people died with an AD-like transcriptome, suggesting they may have been on the path to disease.
A meta-analysis of 2.8 million people estimates 119 in 100,000 develop dementia before age 64—twice the previous estimates. Prevalence increases with age and strikes men and women equally.
B cells in the brain's dura are long-term residents that respond to inflammation.
In an amyloidosis mouse, inhibiting the endosomal proton leak channel NHE6 sped up recycling of ApoE. This slashed amyloid deposition and restored synaptic plasticity.
Single-nucleus RNA sequencing detected microglia, astrocytes, and oligodendrocytes with unique gene expression in late-stage AD brain. Where DNA at transcription factor binding sites was accessible, target gene expression rose.
In carriers of the allele, cognition falters a bit earlier than in noncarriers. Brain amyloid, structure, and metabolism changed, as previously seen in sporadic and familial AD, but only some of the fluid markers did.
Interleukin-3, produced by astrocytes in the brain, helps microglia corral amyloid plaques in Alzheimer’s.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome F. Hoffmann-La Roche, joining our other exhibitors — Biogen, BioLegend, Abcam, BrainXell, and the Jackson Laboratory.
In their quest to understand how gene expression changes in different cell types throughout Alzheimer’s disease, scientists for the first time integrated single-nuclei RNA and ATAC sequencing in the same postmortem brain samples. This enabled them to assess both accessibility and transcription of transcription factors and their respective target genes. The researchers identified AD-specific subsets of brain cells, modeled how they might have become diseased, and linked expressed genes to known GWAS AD risk loci. In oligodendrocytes, the SREP1 transcription factor and its target genes both changed, signaling altered lipid metabolism in AD.
ApoE4 accelerates Alzheimer’s disease in people with Down’s syndrome much like it does in sporadic and familial AD. Compared to noncarriers, cognition faltered on average two years earlier in DS adults harboring the E4 risk allele. Their cortical metabolism slowed, hippocampi shrank, plaque load grew, cerebrospinal fluid Aβ42/40 ratios fell, and plasma phospho-tau181 rose earlier. Surprisingly perhaps, CSF ptau-181, CSF total tau, and fluid neurofilament light did not differ between carriers and noncarriers in this study sample.
- Emory Hill on Amyloid-β positive individuals with subjective cognitive decline present increased CSF neurofilament light levels that relate to lower hippocampal volume.
- Wei Cao on An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging
- Karl Herrup on Do Gene Expression Signatures of Aging Signal AD?
- Andrea Tenner on Do Gene Expression Signatures of Aging Signal AD?
- Andrew E. Budson on Estimates of Young-Onset Dementia Prevalence Just Doubled
- Martin Rossor on Estimates of Young-Onset Dementia Prevalence Just Doubled
- Eric Larson on Estimates of Young-Onset Dementia Prevalence Just Doubled
- Michelle Mielke on Estimates of Young-Onset Dementia Prevalence Just Doubled
- Marco Colonna on More Evidence for Meningeal B Cells
- Jonathan Kipnis and Justin Rustenhoven on More Evidence for Meningeal B Cells
- Nilufer Ertekin-Taner on Single-Cell Transcription Cum Chromatin Analysis Pins SREBF1 to AD
- Marcos Costa on Single-Cell Transcription Cum Chromatin Analysis Pins SREBF1 to AD
- Bradley T. Christian on ApoE4 Hastens Alzheimer’s Disease in Down’s Syndrome
- Andre Strydom on ApoE4 Hastens Alzheimer’s Disease in Down’s Syndrome
- Michael Rafii on ApoE4 Hastens Alzheimer’s Disease in Down’s Syndrome
- Dominic Walsh on Aβ “Receptors” Retard Fibrillization, Enhancing Toxicity
- Arnon Rosenthal and Jenna Pappalardo on Genomic atlas of the proteome from brain, CSF and plasma prioritizes proteins implicated in neurological disorders.
- Steven Estus and Benjamin Shaw on Paper Alert: pQTLs Pin GWAS Loci to Tissue Proteins, Drug Targets
- Benjamin Wolozin on Genomic Double-Stranded RNA: Does C9ORF72 Cause Viral Mimetic Disease?
- Rudy Tanzi on Paper Alert: pQTLs Pin GWAS Loci to Tissue Proteins, Drug Targets
- Baiping Wang and Hui Zheng on Peering Inside Stubby and Mushroom Dendritic Spines