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Comment on the revised FDA Industry Guidance for Early AD Drug Development: Implications for Clinical Outcomes Assessments

Alzheimer’s disease (AD) is characterized by a slow and insidious onset that can last years before impact in daily function is evident. The FDA has required to date that studies in AD demonstrate clinical benefit of new medications in both subjects’ cognitive abilities and functional capacity as a requirement for approval. The three recent drugs that have received FDA approval for AD, Aduhelm, Lequembi, and more recently Kisunla, have demonstrated a slowing in both cognitive and functional decline, in addition to reduction in amyloid burden. Because impairment in functional capacity can take years to become apparent, studies in the preclinical or very early stages of AD would either have to run for years or use efficacy endpoints capable of detecting subtle cognitive changes indicative of slowing or halting disease progression in the absence of functional decline. 

In March 2024, the Food and Drug Administration (FDA) revised its draft guidance for industry entitled “Early Alzheimer’s Disease: Developing Drugs for Treatment”. This guidance applies specifically to trials targeting patients with early sporadic Alzheimer’s disease (AD), prior to the onset of overt dementia. The previous draft guidance published in 2018 required revisions due to the rapidly changing landscape of AD clinical trials, which are increasingly focusing on early disease stages. While cognitive and functional endpoints remain crucial, the 2024 guidance offers more flexibility in their application. Recognizing the challenges in capturing functional changes in early disease stages, the guidance supports the use of sensitive cognitive assessments and other innovative approaches to detect clinically meaningful changes, thus offering a more nuanced understanding of drug efficacy in this context.  

Guidance Summary 

Participants Selection 

In terms of participants’ selection, FDA reiterates its AD staging scheme brought forward in earlier versions of the draft guidance, with Stages ranging from 1 to 6. When designing trials, FDA considers critical to define the target population relying on these Stages. Each Stage varies according to the degree of cognitive complaint, cognitive impairment, and functional impairment. In brief, patients at Stage 1 are asymptomatic, with an absence of subjective or objective cognitive decline and functional impairment. Transition to Stage 2 is characterized by the onset of cognitive symptoms, with patients presenting subjective complaints or detectable cognitive impairment on sensitive neuropsychological tests but no functional impairment. Transition to Stage 3 occurs with the onset of subtle functional impairment, with patients at this stage showing clear impairment on neuropsychological tests as well as mild functional impairment, particularly affecting more complex activities of daily living (ADLs). Finally, Stages 4-6 represent patients with overt dementia and clear functional impairment, with a gradation from mild (Stage 4), to moderate (Stage 5), and severe (Stage 6) dementia. In a clear stance in favor of a biological diagnosis of AD, as opposed to a diagnosis relying on clinical symptoms, all patients categorized under this staging scheme must present biomarker evidence of AD pathophysiological changes. Biomarker testing therefore becomes an essential part of participants’ selection to confirm the AD diagnosis at enrollment and also, possibly, to characterize the presence of comorbid pathologies that could influence the disease presentation and trajectory. Perhaps due to the rapid progress in the development and validation of new biomarkers, FDA does not provide additional guidance on which biomarkers are considered suitable for these purposes.   

Endpoints Selection

The endpoint selection for trials focusing on patients with early AD, with the aim of halting the onset of clinical symptoms or slowing their progression, has unique challenges. By definition, these patients present no to minimal clinical impairment at baseline, complicating the quantification of clinical benefits. Traditionally, drug approval in AD required the assessment of both cognitive and functional impairments, often referred to as the “co-primary” endpoints approach. This approach was adopted to ensure the clinical meaningfulness of reported treatment benefits and remains relevant to trials focusing on later Stages of AD (Stages 3-6) that are accompanied with overt cognitive and functional deficits. However, as previously mentioned, in patients with early AD, it would inevitably lead to trials of unpractically long duration (i.e., 2+ years). Due to the variability in disease trajectories, these trials would also be difficult to plan and execute successfully. In the current guidance, the FDA acknowledges these challenges and demonstrates openness to consider alternative approaches for the evaluation and approval of treatments targeting early AD.   

Historically, effects on cognitive tests alone have not been considered sufficient to support drug approval, due to the questionable clinical meaningfulness of such finding. This revised guidance now recognizes that cognition is essential to daily function and that changes in cognition alone can be clinically meaningful, independent of functional changes which may be more challenging to capture during a trial in this specific population.  Other approaches discussed as potentially appropriate endpoints in early AD trials consists of the use of time-to-event analysis or surrogate markers. Time-to-event analysis aims to detect any drug-related changes in the time to reach a significant milestone in the AD trajectory (e.g., onset of cognitive or functional impairment). The use of surrogate markers has recently been used to support accelerated approval in trials using monoclonal antibodies directed against aggregated forms of beta amyloid. It is important to note that the surrogate endpoint must be “reasonably likely to predict clinical benefit” based on available evidence.  

The appropriateness of endpoints and approval pathways will likely depend on multiple factors, including the characteristics of the study population or the proposed mechanism of action, and early collaboration with FDA during study design will be essential to safeguard trial success.  

Implications for Clinical Outcome Assessments in Early AD Trials 

In recent years, the field of AD has drastically shifted from a diagnosis predominantly based on clinical symptoms (McKhann et al., 2011) to a diagnosis primarily centered around biomarker evidence of AD-related pathophysiological processes, mainly of abnormal aggregation of beta-amyloid (Jack et al., 2018). In this revised industry guidance, the FDA endorses this shift and places the assessment of biomarkers as a central aspect of trials targeting early Alzheimer’s disease, both to support the diagnosis at enrollment and to serve as possible surrogate endpoints to establish treatment efficacy. With the new focus being placed on biomarkers as key outcome in AD trials, questions arise around the role of clinical outcome assessments in these trials.  

Based on FDA’s positions shared in this revised industry guidance, clinical outcome assessments remain essential to AD clinical trials, including those focusing on early disease stages. To start, clinical outcome assessments are needed to appropriately characterize the study population and confirm the AD “stage” of enrolled participants, which requires the assessment of cognitive complaints, objective neuropsychological impairment, and functional impairment.  

In the past, effects on neuropsychological tests alone have not been accepted as lone proof of clinical benefit in absence of functional data. In this version of the draft guidance, FDA shows more openness in considering a significant effect on a neuropsychological test as clinically meaningful for the early AD population. This, however, is dependent on the robustness of the reported effect, with effects of large magnitude and observable across multiple tests or domains being more likely to be deemed sufficient to support drug approval. Sensitive neuropsychological tests thus remains of high relevance to early AD trials, with the implementation of tests assessing multiple cognitive domains and allowing a replication of reported effects being potentially valuable. It is important to note that scales developed to assess cognitive impairment in symptomatic AD trials, such as the ADAS-Cog, are subject to ceiling effects and lack sensitivity in early AD stages. While there is often a reluctance associated with the use of less well-established endpoints, the application of endpoints that might be more sensitive to this population is key in this context.  

Finally, while non-clinical surrogate endpoints are now considered acceptable primary endpoints in early, evidence must support that these endpoints are linked to clinical outcomes. Approval based on non-clinical surrogate markers are likely to require postapproval trials to confirm clinical benefits. Based on positions shared in this revised draft guidance for the industry, clinical outcome assessments remain central to early AD trials, being relevant at different levels, from participants enrollment to efficacy assessment.  

Conclusion 

This newly revised guidance is of high relevance to sponsors planning trials targeting patients with early AD as it outlines FDA’s current position related to key aspects of study design, including participants’ and endpoints’ selection. It aims to streamline early AD drug development by providing clarity on trial design, encouraging earlier intervention, supporting the use of alternative endpoints, and fostering collaboration between sponsors and the agency. The expanded use of biomarkers, acceptance of surrogate endpoints and the introduction of time to event analysis offer new avenues for assessing treatment efficacy. If implemented effectively, this guidance has the potential to accelerate the development of much-needed treatments for Alzheimer’s disease.