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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Center for Neurodegenerative Disease Research, PHILADELPHIA, PA, USA.
Background: Alzheimer's disease (AD) is pathologically defined by the presence of extracellular Aβ plaque and intracellular tau inclusions. Emerging evidence shows that tau aggregates contain pathogenic bioactivities of templating monomeric tau into filamentous fibrils and propagating through cells. Based on these findings, assays have been developed to detect minute amounts of pathogenic tau in human samples.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Penn State University College of Medicine, Hershey, PA, USA.
Background: AD prevention and early interventions require tools for evaluation of people during aging for diagnosis and prognosis of AD conversion. Since AD is a complicated continuum of neurodegenerative processes, developing of such tools have been difficult because it needs longitudinal and multimodal data which are often complicated and incomplete. To address this challenge, we are developing AI4AD framework using ADNI data.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Pittsburgh, Pittsburgh, PA, USA.
Background: The bi-directional autophagy and inflammation network becomes progressively dysregulated with age, with systemic inflammation as a biomarker of this dysregulation including in Alzheimer's Disease (AD). We hypothesize that interventions which target the shared feature of systemic inflammation in the biology of aging and AD, via regulation of the autophagy-inflammation network, will prevent the conversion to disease pathogenesis in AD as well as improve healthspan and longevity in aging populations. While previous studies report benefits of mTOR inhibition including rapamycin in transgenic mouse models of familial AD, the present studies aim to evaluate this pathway in a model of sporadic, late onset AD (LOAD) and test the contribution of AMP-activated protein kinase (AMPK) as a critical regulator of the mTOR pathway.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Background: TDP-43 proteinopathy, initially discovered in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), coexists with tauopathy in a variety of neurodegenerative disorders, including Alzheimer's Disease (AD). While such co-pathology is strongly associated with worsened neurodegeneration and steeper cognitive decline, how these two pathologies influence each other to exacerbate neuron loss remains elusive. That loss of TDP-43 splicing repression occurring in presymptomatic ALS-FTD suggests that loss of TDP-43 function could facilitate the pathological conversion of tau to accelerate tauopathy and neuron loss.
View Article and Find Full Text PDFClinical Manifestations.
Alzheimers Dement
December 2024
Schlegel-UW Research Institute on Aging, Waterloo, ON, Canada.
Background: Multispecialty Interprofessional Team (MINT) Memory Clinics manage dementia care in primary care, allowing for more efficient use of limited specialist resources. This study examined the characteristics of patients on their initial assessment in the MINT clinic and investigated the five-year trajectory of patients with mild cognitive impairment (MCI).
Method: We conducted a retrospective chart review of 751 patients assessed within a MINT Memory Clinic between June 2006 and May 2019 to collect data on age, gender, diagnosis, and MoCA scores.
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