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Journal ArticleDOI

Pathological mechanisms and therapeutic strategies for Alzheimer's disease.

Yaojun Ju, +1 more
- 01 Mar 2022 - 
- Vol. 17, Iss: 3, pp 543-549
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TLDR
A review of representative treatments targeting different pathological pathways currently under clinical evaluations can be found in this paper, where the authors highlight multi-target therapies as an emerging strategy for Alzheimer's disease treatment.
About
This article is published in Neural Regeneration Research.The article was published on 2022-03-01. It has received 110 citations till now. The article focuses on the topics: Disease & Amyloid beta.

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Neurotransmitters—Key Factors in Neurological and Neurodegenerative Disorders of the Central Nervous System

TL;DR: The present paper aims to describe the most important neurotransmitters, broadly classified into canonical (e.g., amino acids, monoamines, acetylcholine, purines, soluble gases, neuropeptides) and noncanonical neurotransmits, and explain their link with some of the most relevant neurological conditions.
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Role of Microglia and Astrocytes in Alzheimer’s Disease: From Neuroinflammation to Ca2+ Homeostasis Dysregulation

TL;DR: An overview of the current understanding of the interactions between the glia cells-mediated inflammatory responses and the molecular mechanisms involved in Ca2+ homeostasis dysregulation in AD is provided.
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Recent advance on carbamate-based cholinesterase inhibitors as potential multifunctional agents against Alzheimer's disease.

TL;DR: Based on the recent research focus on the novel cholinesterase inhibitors with multiple bio-functions, a review aims at summarizing and discussing the most recent studies excavating the potential carbamate-based MTDLs with choline inhibition efficacy, to accelerate the pace of pleiotropic choline-based inhibitors for coping Alzheimer's disease as discussed by the authors .
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New insights into the role and mechanisms of ginsenoside Rg1 in the management of Alzheimer's disease.

TL;DR: In this article , a comprehensive review of the effects and underlying mechanisms of ginsenoside Rg1 on AD has been provided, which shed light on the future directions in the utilization and development of anti-AD drugs.
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Therapeutic Effects of Green Tea Polyphenol (‒)-Epigallocatechin-3-Gallate (EGCG) in Relation to Molecular Pathways Controlling Inflammation, Oxidative Stress, and Apoptosis

TL;DR: The most abundant polyphenol in green tea, Epigallocatechin-3-gallate (EGCG), possesses a wide variety of anti-inflammatory, antioxidant, antifibrotic, anti-remodelation, and tissue-protective properties which may be useful in the treatment of various diseases, particularly in cancer, and neurological, cardiovascular, respiratory, and metabolic disorders as discussed by the authors .
References
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Journal ArticleDOI

Amyloid plaque core protein in Alzheimer disease and Down syndrome

TL;DR: The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy of Alzheimer disease and Down syndrome.
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Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice

TL;DR: Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer β-amyloid (Aβ) precursor protein containing a Lys670 → Asn, Met671 → Leu mutation had normal learning and memory but showed impairment by 9 to 10 months of age.
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Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.

TL;DR: Both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of patients with Alzheimer's disease and 9 neuropathologically normal subjects reveal very powerful correlations with all three psychological assays.
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The amyloid hypothesis of Alzheimer's disease at 25 years

TL;DR: In a recent study, this article showed that low cerebrospinal fluid (CSF) Aβ42 and amyloid-PET positivity precede other AD manifestations by many years.
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Formation of neurofibrillary tangles in P301L tau transgenic mice induced by Aβ42 fibrils

TL;DR: The hypothesis that Aβ42 fibrils can accelerate NFT formation in vivo is supported, and NFTs that contained tau phosphorylated at serine 212/threonine 214 and serine 422 were identified.
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