Alternative therapy of Alzheimer’s disease via supplementation with choline acetyltransferase

Fu, Ai; Li, Qian; Dong, Zhao; Huang, Shi Jie; Wang, Yu Xia; Sun, Mingjun

doi:10.1016/j.neulet.2004.05.116

Cited by 39 publications

(16 citation statements)

References 13 publications

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“…The degree of reduced choline acetyltransferase (ChAT) activity in cerebral cholinergic neurons is significantly correlated with the severity of dementia or cognitive impairment observed in AD [42]. In about half of the AD cases, cortical choline actyltransferase (ChAT) activity was markedly reduced in spite of preserved nucleus basalis of Meynert ChAT activity, suggesting a deficiency of cortical origin and/or of axonal transport in AD [43].…”

Section: Discussionmentioning

confidence: 99%

Feasibility of β-Sheet Breaker Peptide-H102 Treatment for Alzheimer's Disease Based on β-Amyloid Hypothesis

Lin

Tan

et al. 2014

PLoS ONE

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β-amyloid hypothesis is the predominant hypothesis in the study of pathogenesis of Alzheimer's disease. This hypothesis claims that aggregation and neurotoxic effects of amyloid β (Aβ) is the common pathway in a variety of etiological factors for Alzheimer's disease. Aβ peptide derives from amyloid precursor protein (APP). β-sheet breaker peptides can directly prevent and reverse protein misfolding and aggregation in conformational disorders. Based on the stereochemical structure of Aβ1-42 and aggregation character, we had designed a series of β-sheet breaker peptides in our previous work and screened out a 10-residue peptide β-sheet breaker peptide, H102. We evaluated the effects of H102 on expression of P-tau, several associated proteins, inflammatory factors and apoptosis factors, and examined the cognitive ability of APP transgenic mice by behavioral test. This study aims to validate the β-amyloid hypothesis and provide an experimental evidence for the feasibility of H102 treatment for Alzheimer's disease.

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Section: Discussionmentioning

confidence: 99%

Feasibility of β-Sheet Breaker Peptide-H102 Treatment for Alzheimer's Disease Based on β-Amyloid Hypothesis

Lin

Tan

et al. 2014

PLoS ONE

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“…La etanolamina que se obtiene de la fosfatidiletanolamina y la colina que aporta la fosfatidilcolina, son moléculas precursoras de la acetilcolina, el principal neurotransmisor del sistema nervioso central y periférico (30). Actualmente se sugiere la suplementación con colina en aquellas enfermedades que se relacionan con deficiencia de este neurotransmisor, como es el caso de la enfermedad de Alzheimer y Huntington (31,32).…”

Section: Funciones Y Propiedades De Los Fosfolípidosunclassified

Fosfolípidos de origen marino: una nueva alternativa para la suplementación con ácidos grasos omega-3

Sanhueza

et al. 2014

Rev. chil. nutr.

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“…The next step will be to test the application of CPPs in chronic diseases. To our knowledge, only few CPPs have been designed and tested in models of chronic neurodegenerative disease, namely AD [57], PD [55] and amyotrophic lateral sclerosis (ALS) [58]. …”

Section: Cpps In Chronic Neurodegenerative Disordersmentioning

confidence: 99%

Cell Permeable Peptides: A Promising Tool to Deliver Neuroprotective Agents in the Brain

Antoniou

Borsello

2010

Pharmaceuticals

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The inability of most drugs to cross the blood-brain barrier and/or plasma membrane limits their use for biomedical applications in the brain. Cell Permeable Peptides (CPPs) overcome this problem and are effective in vivo, crossing the plasma membrane and the blood-brain barrier. CPPs deliver a wide variety of compounds intracellularly in an active form. In fact, many bioactive cargoes have neuroprotective properties, and due to their ability to block protein-protein interactions, offer exciting perspectives in the clinical setting. In this review we give an overview of the Cell Permeable Peptides strategy to deliver neuroprotectants against neurodegeneration in the CNS.

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Alternative therapy of Alzheimer’s disease via supplementation with choline acetyltransferase

Cited by 39 publications

References 13 publications

Feasibility of β-Sheet Breaker Peptide-H102 Treatment for Alzheimer's Disease Based on β-Amyloid Hypothesis

Feasibility of β-Sheet Breaker Peptide-H102 Treatment for Alzheimer's Disease Based on β-Amyloid Hypothesis

Fosfolípidos de origen marino: una nueva alternativa para la suplementación con ácidos grasos omega-3

Cell Permeable Peptides: A Promising Tool to Deliver Neuroprotective Agents in the Brain

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