Book and manJAD CfP Omics (deadline: July 2023)AIAD Vol.9 (microbiome)gut2022 Alzheimer AwardolfactoryCOVID-19 contentplaqueColverson blogQuiescent HSV-1AIAD Vol.8bvFTDJAD Reports (updated)DW-MRI
Journal of Alzheimer's Disease

is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer's disease.


Upcoming Supplementary Issue: Omics Approaches in Alzheimer's Disease Research (Guest Editor: Sudeshna Das). Click the visual for details in the Calls for Papers (PDF) (opens in a new tab). Submission deadline: July 31, 2023

NEW BOOK: Available for a limited time at a discount

Edited by Giulio M. Pasinetti, this book (AIAD Vol.9) is a compilation of work by researchers intent on exploring the complex role of the gut microbiome in Alzheimer’s disease. For details & to order, click the image or go here

A gut neuroepithelial circuit activation (the neuropod cells) in response to bacterial curli breach in the symptomatic AD mice. TLR2, Toll-Like Receptor 2; Aβ, amyloid-beta; PGP 9.5, Protein gene product 9.5 (neuroendocrine marker). From Das et al., JAD 88(1).

The 2022 Alzheimer Award goes to Yonas E. Geda, MD, and Janina Krell-Roesch, PhD, as co-authors of the winning JAD paper that presents important findings on the impact of physical activity on cognitive change in older adults. For details, go to:

Amyloid-β deposition in the olfactory pathway of WT and App-KI mice: olfactory bulb (OB), anterior olfactory nucleus (AOL), olfactory tubercle (OT), piriform cortex (PC), amygdala (Amg), and entorhinal cortex (EC). From Narukawa et al., JAD88(1).

COVID-19 content in JAD is openly available. Read all content including the editorial by JAD's Editor-in-Chief George Perry, in which he calls out for careful study to determine the numbers of AD patients infected and dying of COVID-19, via:

G) A compact plaque double stained with anti-Aβ antibody W02 (red) and DAPI with 0.3% Sudan Black pretreatment to remove autofluorescence. H) The compact Aβ (arrows) remains DAPI-positive despite pretreatment, showing that DAPI stains compact plaques. From Mabrouk et al., JAD88(3).

Familiar Music May Help Caregivers and Loved Ones Living with Dementia to Connect with One Another

by Aaron Colverson

Quiescent HSV-1 is reactivated by VZV infection to cause AD. (A) VCV-induced quiescence of HSV-1 shown by expression of LAT. VZV infection after HSV-1 latency confirmed by qPCR. HSV and VZV (B) and Aβ and TUJ1 expression (C) detected via immunostaining. From Cairns et al., JAD88(3).

This new book, edited by Lilian Calderón-Garcidueñas, is a compilation of work by researchers intent on revealing the links between air pollution and neurodegeneration. For details & to order, click the image or go here

A 25-year-old patient experienced an extremely early onset of bvFTD with frontal-temporal atrophy on T1 and hypometabolism on FDG-PET, however, no Aβ and tau protein deposition was found on AV45 and PI2620 PET. From Chu et al., JAD90(3).

JAD Reports is our fully open access international, multidisciplinary journal dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer's disease. View new content

Analysis of multi-shell DW-MRI reveals significant effects of disease stage on diffusion-derived measures of tissue integrity. Specific WM tracts show decreased apparent fiber density (AFD) and fiber bundle cross-section (FC). From Giraldo et al., JAD90(4).



24 May 2023

Case Study Reveals Potentially Lethal Side Effects of Lecanemab for Treatment of Alzheimer's Disease

In a noteworthy case study published in the Journal of Alzheimer’s Disease investigators report autopsy findings in a 65-year-old woman with Alzheimer’s disease (AD) who received three open label infusions of the experimental anti-amyloid beta (Aβ) antibody drug lecanemab. Four days after the last infusion, she experienced stroke symptoms and died several days later due to multifocal intracerebral hemorrhage despite attempts at therapeutic intervention. Neuropathologic findings reflected therapy-induced Aβ phagocytosis involving fibrillar Aβ both in the parenchymal brain tissue and in the cerebral vasculature.

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