Alzheimer's, Parkinson's & Neurodegeneration

Anti-amyloid antibodies, plasma p-tau biomarkers, alpha-synuclein seed amplification, antisense therapies for ALS and emerging disease-modifying strategies.

355 papersnewest Oct 28, 2026

Most influential

  • Lecanemab in Early Alzheimer’s Disease
    Article5,673 citationsdoi:10.1056/nejmoa2212948
  • Recent advances in Alzheimer’s disease: mechanisms, clinical trials and new drug development strategies

    Alzheimer's disease (AD) stands as the predominant form of dementia, presenting significant and escalating global challenges. Its etiology is intricate and diverse, stemming from a combination of factors such as aging, genetics, and environment. Our current understanding of AD pathologies involves various hypotheses, such as the cholinergic, amyloid, tau pro…

    Abstract excerpt by Jifa Zhang et al., CC-BY, https://doi.org/10.1038/s41392-024-01911-3; truncated.

    Review1,176 citationsdoi:10.1038/s41392-024-01911-3
  • Diagnostic Accuracy of a Plasma Phosphorylated Tau 217 Immunoassay for Alzheimer Disease Pathology

    Importance Phosphorylated tau (p-tau) is a specific blood biomarker for Alzheimer disease (AD) pathology, with p-tau217 considered to have the most utility. However, availability of p-tau217 tests for research and clinical use has been limited. Expanding access to this highly accurate AD biomarker is crucial for wider evaluation and implementation of AD bloo…

    Abstract excerpt by Ashton NJ et al., CC-BY, https://doi.org/10.1001/jamaneurol.2023.5319; truncated.

    Article770 citationsdoi:10.1001/jamaneurol.2023.5319
  • Lecanemab: Appropriate Use Recommendations

    Lecanemab (Leqembi®) is approved in the United States for the treatment of Alzheimer's disease (AD) to be initiated in early AD (mild cognitive impairment [MCI] due to AD or mild AD dementia) with confirmed brain amyloid pathology. Appropriate Use Recommendations (AURs) are intended to help guide the introduction of new therapies into real-world clinical pra…

    Abstract excerpt by Jeffrey L. Cummings et al., CC-BY, https://doi.org/10.14283/jpad.2023.30; truncated.

    Article960 citationsdoi:10.14283/jpad.2023.30
  • A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer’s disease with lecanemab, an anti-Aβ protofibril antibody

    BACKGROUND: Lecanemab (BAN2401), an IgG1 monoclonal antibody, preferentially targets soluble aggregated amyloid beta (Aβ), with activity across oligomers, protofibrils, and insoluble fibrils. BAN2401-G000-201, a randomized double-blind clinical trial, utilized a Bayesian design with response-adaptive randomization to assess 3 doses across 2 regimens of lecan…

    Abstract excerpt by Chad J. Swanson et al., CC-BY, https://doi.org/10.1186/s13195-021-00813-8; truncated.

    Article844 citationsdoi:10.1186/s13195-021-00813-8
  • Highly accurate blood test for Alzheimer's disease is similar or superior to clinical cerebrospinal fluid tests

    With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. In this study, we evaluated whether a precise blood test could perform as well as established cerebrospinal fluid (CSF) tests in detecting amyloid-β (Aβ) plaques and tau tangles. Plasma %p-tau217 (ratio of…

    Abstract excerpt by Barthélemy NR et al., CC-BY, https://doi.org/10.1038/s41591-024-02869-z; truncated.

    Article449 citationsdoi:10.1038/s41591-024-02869-z
  • Plasma p-tau231: a new biomarker for incipient Alzheimer's disease pathology

    The quantification of phosphorylated tau in biofluids, either cerebrospinal fluid (CSF) or plasma, has shown great promise in detecting Alzheimer's disease (AD) pathophysiology. Tau phosphorylated at threonine 231 (p-tau231) is one such biomarker in CSF but its usefulness as a blood biomarker is currently unknown. Here, we developed an ultrasensitive Single …

    Abstract excerpt by Ashton NJ et al., CC-BY, https://doi.org/10.1007/s00401-021-02275-6; truncated.

    Article615 citationsdoi:10.1007/s00401-021-02275-6
  • Plasma p-tau231 and p-tau217 as state markers of amyloid-β pathology in preclinical Alzheimer's disease

    Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. Previous biofluid data suggest that phosphorylated tau231 (p-tau231) could indicate incipient Aβ pathology, but a comprehensive comparison with other putative bloo…

    Abstract excerpt by Milà-Alomà M et al., CC-BY, https://doi.org/10.1038/s41591-022-01925-w; truncated.

    Article534 citationsdoi:10.1038/s41591-022-01925-w
  • Anti-Amyloid Monoclonal Antibodies for the Treatment of Alzheimer’s Disease
    Review377 citationsdoi:10.1007/s40259-023-00633-2
  • Lecanemab, Aducanumab, and Gantenerumab — Binding Profiles to Different Forms of Amyloid-Beta Might Explain Efficacy and Side Effects in Clinical Trials for Alzheimer's Disease

    Immunotherapy against amyloid-beta (Aβ) is a promising option for the treatment of Alzheimer's disease (AD). Aβ exists as various species, including monomers, oligomers, protofibrils, and insoluble fibrils in plaques. Oligomers and protofibrils have been shown to be toxic, and removal of these aggregates might represent an effective treatment for AD. We have…

    Abstract excerpt by Linda Söderberg et al., CC-BY, https://doi.org/10.1007/s13311-022-01308-6; truncated.

    Article433 citationsdoi:10.1007/s13311-022-01308-6
  • Differential roles of Aβ42/40, p-tau231 and p-tau217 for Alzheimer's trial selection and disease monitoring

    Blood biomarkers indicative of Alzheimer's disease (AD) pathology are altered in both preclinical and symptomatic stages of the disease. Distinctive biomarkers may be optimal for the identification of AD pathology or monitoring of disease progression. Blood biomarkers that correlate with changes in cognition and atrophy during the course of the disease could…

    Abstract excerpt by Ashton NJ et al., CC-BY, https://doi.org/10.1038/s41591-022-02074-w; truncated.

    Article420 citationsdoi:10.1038/s41591-022-02074-w
  • Lecanemab in patients with early Alzheimer’s disease: detailed results on biomarker, cognitive, and clinical effects from the randomized and open-label extension of the phase 2 proof-of-concept study

    BACKGROUND: Lecanemab, a humanized IgG1 monoclonal antibody that targets soluble aggregated Aβ species (protofibrils), has demonstrated robust brain fibrillar amyloid reduction and slowing of clinical decline in early AD. The objective of this analysis is to report results from study 201 blinded period (core), the open-label extension (OLE), and gap period (…

    Abstract excerpt by Eric McDade et al., CC-BY, https://doi.org/10.1186/s13195-022-01124-2; truncated.

    Article306 citationsdoi:10.1186/s13195-022-01124-2
  • The AHEAD 3‐45 Study: Design of a prevention trial for Alzheimer's disease
    Article291 citationsdoi:10.1002/alz.12748
  • Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update

    Alzheimer's disease (AD) is the leading cause of dementia, presenting a significant unmet medical need worldwide. The pathogenesis of AD involves various pathophysiological events, including the accumulation of amyloid and tau, neuro-inflammation, and neuronal injury. Clinical trials focusing on new drugs for AD were documented in 2020, but subsequent develo…

    Abstract excerpt by Li‐Kai Huang et al., CC-BY, https://doi.org/10.1186/s12929-023-00976-6; truncated.

    Review252 citationsdoi:10.1186/s12929-023-00976-6
  • Prediction of Longitudinal Cognitive Decline in Preclinical Alzheimer Disease Using Plasma Biomarkers

    Importance Alzheimer disease (AD) pathology starts with a prolonged phase of β-amyloid (Aβ) accumulation without symptoms. The duration of this phase differs greatly among individuals. While this disease phase has high relevance for clinical trial designs, it is currently unclear how to best predict the onset of clinical progression. Objective To evaluate co…

    Abstract excerpt by Mattsson-Carlgren N et al., CC-BY, https://doi.org/10.1001/jamaneurol.2022.5272; truncated.

    Article295 citationsdoi:10.1001/jamaneurol.2022.5272

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