Plasma neurofilament L to amyloid β42 ratio in differentiating Alzheimer’s type from non-Alzheimer’s dementia: A cross-sectional pilot study from India

Subramanian, S.; Krishna, Geethu; Sivakumar, Palanimuthu T.; Dahale, Ajit Bhalchandra; J, Susheel Kumar; Sinha, Preeti; Varghese, Mathew

doi:10.1016/j.ajp.2021.102914

Cited by 7 publications

(5 citation statements)

References 19 publications

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“…As neurotransmitter regulators, these drugs can relieve symptoms for a short time but cannot delay the progression of AD [ 30 ]. Recently, a new drug, aducanumab, has been sent to the FDA after analysis yielded positive results in early Alzheimer's disease [ 31 ]. Donepezil is a representative cholinesterase inhibitor that improves the ability of impaired nerve endings to transmit messages between nerve cells [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

The Combination of β‐Asarone and Icariin Inhibits Amyloid‐β and Reverses Cognitive Deficits by Promoting Mitophagy in Models of Alzheimer’s Disease

Wang

Pan

et al. 2021

Oxidative Medicine and Cellular Longevity

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β-Asarone is the main constituent of Acorus tatarinowii Schott and exhibits important effects in diseases such as neurodegenerative and neurovascular diseases. Icariin (ICA) is a major active ingredient of Epimedium that has attracted increasing attention because of its unique pharmacological effects in degenerative disease. In this paper, we primarily explored the effects of the combination of β-asarone and ICA in clearing noxious proteins and reversing cognitive deficits. The accumulation of damaged mitochondria and mitophagy are hallmarks of aging and age-related neurodegeneration, including Alzheimer’s disease (AD). Here, we provide evidence that autophagy/mitophagy is impaired in the hippocampus of APP/PS1 mice and in Aβ1-42-induced PC12 cell models. Enhanced mitophagic activity has been reported to promote Aβ and tau clearance in in vitro and in vivo models. Meanwhile, there is growing evidence that treatment of AD should be preceded by intervention before the formation of pathological products. The efficacy of the combination therapy was better than that of the individual therapies applied separately. Then, we found that the combination therapy also inhibited cell and mitochondrial damage by inducing autophagy/mitophagy. These findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis, and that combination treatment with mitophagy inducers represents a potential strategy for therapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

The Combination of β‐Asarone and Icariin Inhibits Amyloid‐β and Reverses Cognitive Deficits by Promoting Mitophagy in Models of Alzheimer’s Disease

Wang

Pan

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Written informed consent was obtained from all participants. The criteria followed for selection of participants and clinical assessment scales administered are previously described [ 5 ]. In brief, NIA-AA criteria for selection of AD subjects, ICD-10 and NIA-AA criteria for selection of NAD subjects were followed.…”

Section: Methodsmentioning

confidence: 99%

“…The quantification of NfL, Aβ 42 , and p-tau 181 using Simoa HD-X analyzer has been described earlier [ 5 ]. Additionally, t-tau in plasma was measured using Simoa assay kit for t-tau (#101552) following the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

Potential Utility of Plasma Biomarker Panels in Differential Diagnosis of Alzheimer’s Disease

Krishna,

Thangaraju Sivakumar,

Dahale

et al. 2024

Journal of Alzheimer's Disease Reports

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Blood tests are in need, in the clinical diagnosis of Alzheimer’s disease (AD) as minimally invasive and less expensive alternatives to cerebrospinal fluid and neuroimaging methods. On these lines, single molecule array (Simoa) analysis of amyloid-β (Aβ42), total tau (t-tau), phospho-tau (p-tau 181), and neurofilament L (NfL) in the plasma samples of AD subjects, healthy controls (HC), and non-AD subjects was conducted. Findings from this study suggest that a panel of multiple plasma biomarkers (NfL, Aβ42, t-tau, and p-tau 181) combined with the clinical assessments could support differential diagnosis of AD and other dementias from healthy controls.

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“…Written informed consent was obtained from all participants. The socio-demographic details of the participants and S389 the criteria followed for their selection and clinical assessment scores are described earlier [17].…”

Section: Subjectsmentioning

confidence: 99%

Pathological (Dis)Similarities in Neuronal Exosome-Derived Synaptic and Organellar Marker Levels Between Alzheimer’s Disease and Frontotemporal Dementia

Krishna

Santhoshkumar

Sivakumar

et al. 2023

JAD

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Background: Alzheimer’s disease (AD) and frontotemporal dementia (FTD) are pathologically distinct neurodegenerative disorders with certain overlap in cognitive and behavioral symptoms. Both AD and FTD are characterized by synaptic loss and accumulation of misfolded proteins, albeit, in different regions of the brain. Objective: To investigate the synaptic and organellar markers in AD and FTD through assessment of the levels of synaptic protein, neurogranin (Ng) and organellar proteins, mitofusin-2 (MFN-2), lysosomal associated membrane protein-2 (LAMP-2), and golgin A4 from neuronal exosomes. Methods: Exosomes isolated from the plasma of healthy controls (HC), AD and FTD subjects were characterized using transmission electron microscopy. Neurodegenerative status was assessed by measurement of neurofilament light chain (NfL) using Simoa. The pooled exosomal extracts from each group were analyzed for Ng, MFN-2, LAMP-2, and golgin A4 by western blot analysis using enhanced chemiluminescence method of detection. Results: The densitometric analysis of immunoreactive bands demonstrated a 65% reduction of Ng in AD and 53% in FTD. Mitochondrial protein MFN-2 showed a significant reduction by 32% in AD and 46% in FTD. Lysosomal LAMP-2 and Golgi complex associated golgin A4 were considerably increased in both AD and FTD. Conclusion: Changes in Ng may reflect the ongoing synaptic degeneration that are linked to cognitive disturbances in AD and FTD. Importantly, the rate of synaptic degeneration was more pronounced in AD. Changes to a similar extent in both the dementia groups in organellar proteins indicates shared mechanisms of protein accumulation/degradation common to both AD and FTD.

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Plasma neurofilament L to amyloid β42 ratio in differentiating Alzheimer’s type from non-Alzheimer’s dementia: A cross-sectional pilot study from India

Cited by 7 publications

References 19 publications

The Combination of β‐Asarone and Icariin Inhibits Amyloid‐β and Reverses Cognitive Deficits by Promoting Mitophagy in Models of Alzheimer’s Disease

The Combination of β‐Asarone and Icariin Inhibits Amyloid‐β and Reverses Cognitive Deficits by Promoting Mitophagy in Models of Alzheimer’s Disease

Potential Utility of Plasma Biomarker Panels in Differential Diagnosis of Alzheimer’s Disease

Pathological (Dis)Similarities in Neuronal Exosome-Derived Synaptic and Organellar Marker Levels Between Alzheimer’s Disease and Frontotemporal Dementia

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