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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami Miller School of Medicine, Miami, FL, USA.
Background: Common and rare variants in SORL1 have been associated with increased risk of Alzheimer's disease (AD). Since 2019, we have run an international collaborative research initiative to ascertain a Peruvian cohort for Alzheimer's disease and other related dementias for genetic studies (PeADI).
Method: A Peruvian family (4 AD cases and two mild cognitive impairment (MCI) cases) was recruited through the PeADI study.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Background: The infectious hypothesis of Alzheimer's disease (AD) suggests that microbes may play a role in pathogenesis by triggering the pathologic cascade or contributing to disease progression. Herpesviruses, such as Epstein-Barr virus (EBV), have been of high interest in AD and related neurodegenerative diseases, in part due to their ability to establish lifelong latent infection and potentially reactivate. However, further research is needed to fully understand the role of herpesviruses in these diseases.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Washington University School of Medicine, St. Louis, MO, USA.
Background: P-tau217 has emerged as a compelling alternative to long-established p-tau181 to accurately measure tau modifications in biofluids in response to brain Abeta and tau deposition in Alzheimer's disease (AD). Understanding the specificity and significance of p-tau217 changes over AD stages is critical to interpret its potential response to treatments against Abeta and tau aggregation.
Methods: We measured p-tau217 phosphorylation by mass spectrometry.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
The Neurodegeneration Consortium, UT MD Anderson Cancer Center, Houston, TX, USA.
Background: Chemotherapy-induced cognitive impairment (CICI) is a commonly reported neurotoxic side effect of chemotherapy, occurring in up to 75% cancer patients. Connections between chemo-treatment and increased risk of dementia have been reported. Mechanistically, chemotherapy treatment contributes to an accelerated aging phenotype in the brain through induction of pathogenic tau, disruption of neuronal integrity, reactive gliosis and neuroinflammation.
View Article and Find Full Text PDFClinical Manifestations.
Alzheimers Dement
December 2024
Faculty of Health, Medicine and Life Sciences, School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, Maastricht, The Netherlands, Maastricht, Netherlands; Gordon Center for Medical Imaging, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA.
Background: The brainstem locus coeruleus (LC) is among the first sites of Alzheimer's disease (AD) pathology, accruing hyperphosphorylated tau as early as in young adulthood. Animal studies indicate that the LC is crucially involved in sleep-wake regulation, a recently established factor contributing to AD-related pathophysiological processes. However, the associations between LC integrity and sleep-wake phenotypes in the context of AD pathology remain poorly characterized in humans.
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