Journal 2018 and manWhat is Abeta?BMDMLtauQSM and PETJAD Reportscytoplasmtemporal cortexABCA7
The Journal of Alzheimer's Disease

celebrates its 20th anniversary in 2018. The special open access celebratory issue (Vol. 62, Iss.3) features 35 review articles covering 20 years of Alzheimer's disease research, plus personal perspectives from researchers in the field.

READ ISSUE HERE

LATEST JAD EDITORS’ BLOG
What is Aβ?
by Sally Hunter

In hippocampus of a mouse model of Alzheimer’s disease receiving transplantation with bone-marrow-derived microglia-like (BMDML) cells, BMDML cells were co-localized with Aβ (arrows). Z-stack image clearly indicates Aβ phagocytosis by BMDML cells. From Kawanishi et al., JAD64(2).

Plaques of patients with Alzheimer’s disease can be visualized with both Methoxy-X04 staining (blue) and antibodies against hyperphosphorylated tau protein (PHF-Tau) isoforms, as PHF-Tau-pS396 (green) and PHF-Tau-AT8 (red). From Furcila et al., JAD64(2).

QSM and Aβ-PET in fusion with T1-weighted MRI of a Alzheimer’s disease (AD) patient and a healthy control (HC) showing higher susceptibility for AD patient in globus pallidus, but not in cortical areas despite a higher PET signal. From Tiepolt et al., JAD64(2).

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

Translocated I2PP2A/SET (green) is colocalized with hyperphosphorylated tau (red) in the neuronal (nuclei, blue, TOPRO) cytoplasm in cerebral cortex of 3xTg-AD mice with traumatic brain injury. From Hu et al., JAD64(3).

In temporal cortex tissue from a representative Alzheimer’s disease patient, the receptor for advanced glycation endproducts (RAGE) is highly expressed in IBA1-expressing myeloid cells. Code: RAGE, green; IBA1, red; DAPI, blue; and far right panel (yellow), merge. From Derk et al., JAD 64(3).

SiRNA technique has been used to decrease ABCA7 expression in murine endothelial cells reproducing the blood-brain barrier in vitro. ABCA7 deficiency does not disrupt expression and localisation of tight junction proteins. From Lamartinière et al., JAD64(4).

Welcome to Journal of Alzheimer's Disease

Journal Ranking

Journal Ranking

The 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. The journal publishes research reports, reviews, short communications, hypotheses, ethics reviews, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer's disease.

JAD has an Impact Factor of 3.731 (2017 Journal Citation Reports), an h-index of 87 (Web of Science), an h-index of 85 (SCImago Journal Rank indicator), an h5-index of 62 (Google Scholar), and an h5-median of 78 (Google Scholar).

No front page content has been created yet.