Publications by authors named "S Abushakra"
Article Synopsis
- The APOLLOE4 trial is a Phase 3 study evaluating the safety and efficacy of the oral drug ALZ-801 in patients with early Alzheimer's disease (AD) who possess the high-risk apolipoprotein E ε4/ε4 genotype.
- It enrolled 325 subjects aged 50-80, primarily with mild cognitive impairment, and aims to show a significant difference in cognitive function compared to a placebo over 78 weeks.
- Expected topline results in 2024 could provide insights into ALZ-801 as a potential first effective treatment for this high-risk group.
Introduction: ALZ-801/valiltramiprosate is an oral, small-molecule inhibitor of beta-amyloid (Aβ) aggregation and oligomer formation in late-stage development as a disease-modifying therapy for early Alzheimer's disease (AD). The present investigation provides a quantitative systems pharmacology (QSP) analysis of amyloid fluid biomarkers and cognitive results from a 2-year ALZ-801 Phase 2 trial in APOE4 carriers with early AD.
Methods: The single-arm, open-label phase 2 study evaluated effects of ALZ-801 265 mg two times daily (BID) on cerebrospinal fluid (CSF) and plasma amyloid fluid biomarkers over 104 weeks in APOE4 carriers with early AD [Mini-Mental State Examination (MMSE) ≥ 22].
Introduction: ALZ-801/valiltramiprosate is a small-molecule oral inhibitor of beta amyloid (Aβ) aggregation and oligomer formation being studied in a phase 2 trial in APOE4 carriers with early Alzheimer's disease (AD) to evaluate treatment effects on fluid and imaging biomarkers and cognitive assessments.
Methods: The single-arm, open-label phase 2 trial was designed to evaluate the effects of the ALZ-801 265 mg tablet taken twice daily (after 2 weeks once daily) on plasma fluid AD biomarkers, hippocampal volume (HV), and cognition over 104 weeks in APOE4 carriers. The study enrolled subjects aged 50-80 years, with early AD [Mini-Mental State Examination (MMSE) ≥ 22, Clinical Dementia Rating-Global (CDR-G) 0.
Article Synopsis
- New research indicates that the aggregation of misfolded proteins is a key factor in the development of Alzheimer's disease (AD) and similar neurodegenerative disorders, leading to a new theory of brain degeneration.
- Genetic evidence highlights soluble beta-amyloid aggregates as the main neurotoxin responsible for the onset and progression of AD, rather than the larger, less reactive amyloid plaques.
- Understanding the harmful effects of these soluble aggregates (oligomers and protofibrils) is crucial for developing effective treatments that can address the root causes of neurodegeneration in AD and other related diseases.