Prodromes in demyelinating disorders, amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer's dementia

Marrie, Ruth Ann; Maxwell, Colleen J.; Rotstein, Dalia; Tsai, Chih Cheng; Tremlett, Helen

doi:10.1016/j.neurol.2023.07.002

Revue Neurologique

2024

DOI: 10.1016/j.neurol.2023.07.002

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Prodromes in demyelinating disorders, amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer's dementia

Ruth Ann Marrie

Colleen J. Maxwell

Dalia Rotstein

et al.

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2024

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Cited by 3 publications

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“…In the case of Alzheimer's disease (AD), neuropathological changes start one to two decades prior to the manifestation of cognitive decline and/or clinical diagnosis of dementia (Marrie et al, 2023 ). Early synaptic dysfunction and its resultant altered oscillatory activity in various neuromodulatory networks have been proposed as potential prodromal changes of Alzheimer's pathology (Pelucchi et al, 2022 ).…”

mentioning

confidence: 99%

Editorial: Prodromal stage of neurodegenerative proteinopathies: from bench to bedside

Xu,

Fereshtehnejad,

Zeighami

2023

Front. Neurosci.

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mentioning

confidence: 99%

Editorial: Prodromal stage of neurodegenerative proteinopathies: from bench to bedside

Xu,

Fereshtehnejad,

Zeighami

2023

Front. Neurosci.

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Is there a prodrome to NMOSD? An investigation of neurologic symptoms preceding the first NMOSD attack

Lee,

Marrie,

Fadda

et al. 2024

Mult Scler

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Background: It is unknown whether people with aquaporin-4 antibody positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) experience a prodrome, although a few cases report AQP4 + serology up to 16 years before the first attack. Objectives: To evaluate whether individuals with AQP4-IgG + NMOSD have prodromal neurologic symptoms preceding the first attack. Methods: We reviewed medical records of participants meeting the 2015 diagnostic criteria for AQP4-IgG + NMOSD from four demyelinating disease centres in the Canadian NMOSD cohort study CANOPTICS. We searched for neurologic symptoms occurring at least 30 days before the first attack. Results: Of 116 participants with NMOSD, 17 (14.7%) had prodromal neurologic symptoms. The median age was 48 years (range 25–83) at first attack; 16 (94.1%) were female. Participants presented with numbness/tingling ( n = 9), neuropathic pain ( n = 5), visual disturbance ( n = 4), tonic spasms ( n = 2), Lhermitte sign ( n = 2), severe headache ( n = 2), incoordination ( n = 2), weakness ( n = 1), psychosis ( n = 1) or seizure ( n = 1). Of eight who underwent magnetic resonance imaging (MRI) brain, orbits and/or spinal cord, five had T2 lesions. Within 1.5–245 months (median 14) from the onset of prodromal neurologic symptoms, participants experienced their first NMOSD attack. Conclusions: One in seven people with NMOSD experienced neurologic symptoms before their first attack. Further investigation of a possible NMOSD prodrome is warranted.

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Considering Biomarkers of Neurodegeneration in Alzheimer’s Disease: The Potential of Circulating Cell-Free DNA in Precision Neurology

Pollard,

Saito,

Burns

et al. 2024

JPM

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Neurodegenerative diseases, such as Alzheimer’s disease (AD), are a growing public health crisis, exacerbated by an aging global population and the lack of effective early disease-modifying therapies. Early detection of neurodegenerative disorders is critical to delaying symptom onset and mitigating disease progression, but current diagnostic tools often rely on detecting pathology once clinical symptoms have emerged and significant neuronal damage has already occurred. While disease-specific biomarkers, such as amyloid-beta and tau in AD, offer precise insights, they are too limited in scope for broader neurodegeneration screening for these conditions. Conversely, general biomarkers like neurofilament light chain (NfL) provide valuable staging information but lack targeted insights. Circulating cell-free DNA (cfDNA), released during cell death, is emerging as a promising biomarker for early detection. Derived from dying cells, cfDNA can capture both general neurodegenerative signals and disease-specific insights, offering multi-layered genomic and epigenomic information. Though its clinical potential remains under investigation, advances in cfDNA detection sensitivity, standardized protocols, and reference ranges could establish cfDNA as a valuable tool for early screening. cfDNA methylation signatures, in particular, show great promise for identifying tissue-of-origin and disease-specific changes, offering a minimally invasive biomarker that could transform precision neurology. However, further research is required to address technological challenges and validate cfDNA’s utility in clinical settings. Here, we review recent work assessing cfDNA as a potential early biomarker in AD. With continued advances, cfDNA could play a pivotal role in shifting care from reactive to proactive, improving diagnostic timelines and patient outcomes.

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Prodromes in demyelinating disorders, amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer's dementia

Cited by 3 publications

References 149 publications

Editorial: Prodromal stage of neurodegenerative proteinopathies: from bench to bedside

Editorial: Prodromal stage of neurodegenerative proteinopathies: from bench to bedside

Is there a prodrome to NMOSD? An investigation of neurologic symptoms preceding the first NMOSD attack

Considering Biomarkers of Neurodegeneration in Alzheimer’s Disease: The Potential of Circulating Cell-Free DNA in Precision Neurology

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