Review
Biochemistry & Molecular Biology
Ruifeng Zhang, Miao Zeng, Xiaolu Zhang, Yujia Zheng, Nuan Lv, Luming Wang, Jiali Gan, Yawen Li, Xijuan Jiang, Lin Yang
Summary: Saponins, specifically ginsenoside Rg1 and pseudoginsenoside-F11, show the most promise in treating Alzheimer's disease by reducing amyloid beta peptide deposition, inhibiting tau phosphorylation, modulating oxidative stress, reducing inflammation, and antiapoptosis. This review provides a comprehensive summary and classification of common saponins studied for their therapeutic potential in Alzheimer's disease, showcasing their underlying mechanisms.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Elena Tamagno, Michela Guglielmotto, Valeria Vasciaveo, Massimo Tabaton
Summary: The pathogenesis of Alzheimer's disease involves the accumulation of beta amyloid and vulnerability of the brain to oxidative stress, which are linked to each other. It is difficult to determine which comes first, Aβ or oxidative stress. Evidence suggests that oxidative stress occurs early in the development of Alzheimer's disease and plays a crucial role in the manifestation of clinical and pathological symptoms.
Review
Chemistry, Applied
Zhiyuan Zhang, Shuai Wang, Haining Tan, Pei Yang, Yuanyuan Li, Lingchuan Xu, Baoguo Duan, Yuhong Liu
Summary: This paper reviews recent research on the regulation of natural polysaccharides in Alzheimer's disease (AD) and systematically lists possible intervention pathways of polysaccharides targeting different mechanisms.
CARBOHYDRATE POLYMERS
(2022)
Article
Biochemistry & Molecular Biology
Ratnakar Jadhav, Yogesh A. Kulkarni
Summary: Alzheimer's disease is a neurodegenerative condition characterized by progressive loss of memory and cognitive dysfunction, particularly in older individuals. The prevalence of the disease has increased due to the global aging population. Current treatments for Alzheimer's disease have limited efficacy and adverse effects. Recent research suggests that natural products, such as baicalein, could be potential treatment options for Alzheimer's disease. Baicalein, a flavonoid from the flavone subclass, has shown neuroprotective properties through its antioxidant, anti-inflammatory, AChE enzyme inhibitory, and anti-amyloid protein aggregation activities.
Review
Biochemistry & Molecular Biology
Andrila E. Collins, Tarek M. Saleh, Bettina E. Kalisch
Summary: The prevalence of Alzheimer's disease is estimated to double by 2040. Current treatments do not address the underlying causes of the disease, but research suggests that antioxidants may help mitigate oxidative stress. Recent studies have focused on natural antioxidants as potential preventatives and treatments for neurodegenerative conditions associated with oxidative stress.
Article
Neurosciences
Dongjie Hu, Xiangjun Dong, Qunxian Wang, Mingjing Liu, Shuyue Luo, Zijun Meng, Zijuan Feng, Weihui Zhou, Weihong Song
Summary: This study explores the role of Purkinje cell protein 4 (PCP4) in the progression of Alzheimer's disease (AD). PCP4 overexpression affects the processing of amyloid-beta protein precursor (AβPP) and promotes the production and deposition of amyloid-beta (Aβ). It also exacerbates learning and memory impairment in AD model mice. PCP4 may serve as a potential therapeutic target for AD by targeting Aβ pathology.
JOURNAL OF ALZHEIMERS DISEASE
(2023)
Article
Immunology
Liu Yang, Huimin Zhou, Lei Huang, Yong Su, Liangliang Kong, Pengmin Ji, Ran Sun, Chao Wang, Weiping Li, Weizu Li
Summary: Chronic glucocorticoid exposure can accelerate neuronal damage and beta-amyloid production by activating oxidative stress and NLRP1 inflammasome, leading to the deterioration of Alzheimer's disease. Inhibition of NLRP1 inflammasome may be an important strategy in improving chronic glucocorticoid-induced neuronal injury.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Yun Ding, Xin Wang, Jing Ji, Xuejiao Zhang, Mengdi Chen, Shuling Li, Qiongyao Zhang, Ping Liu
Summary: Our study investigated the protective effects of a novel glycogen synthase kinase-3 beta (GSK-3 beta) inhibitor, 9b, on the learning and memory function of rats with amyloid-beta(1-42) induced Alzheimer's disease (AD), showing that 9b improved learning and memory dysfunction through antioxidant and antiapoptotic effects, regulating neurotransmitter concentrations and reducing brain damage caused by amyloid-beta(1-42).
ACS CHEMICAL NEUROSCIENCE
(2021)
Review
Nutrition & Dietetics
Gong Peng, Ming Li, Zhaoli Meng
Summary: Alzheimer's disease is a devastating disease with no disease-modified treatment discovered yet. Recent studies have shown that polysaccharides potentially have benefits in alleviating the pathological damage and improving cognitive symptoms of Alzheimer's disease, but further research is needed.
FRONTIERS IN NUTRITION
(2023)
Article
Chemistry, Multidisciplinary
Xin Chen, Santosh Pandit, Lei Shi, Vaishnavi Ravikumar, Julie Bonne Kohler, Ema Svetlicic, Zhejian Cao, Abhroop Garg, Dina Petranovic, Ivan Mijakovic
Summary: Alzheimer's disease is a common neurodegenerative disease characterized by the aggregation of misfolded amyloid-beta peptides in the brain. Graphene oxide nanoflakes have been found to effectively inhibit A beta aggregation in vitro. In this study using yeast as a model, it is shown that graphene oxide can penetrate yeast cells and reduce A beta 42 toxicity. The findings provide insights for designing graphene oxide-based therapies for attenuating cytotoxicity of A beta 42 and other misfolded proteins involved in neurodegenerative pathology.
ADVANCED FUNCTIONAL MATERIALS
(2023)
Article
Neuroimaging
Austin M. Bazydlo, Matthew D. Zammit, Minjie Wu, Patrick J. Lao, Douglas C. Dean, Sterling C. Johnson, Dana L. Tudorascu, Ann Cohen, Karly A. Cody, Beau Ances, Charles M. Laymon, William E. Klunk, Shahid Zaman, Benjamin L. Handen, Sigan L. Hartley, Andrew L. Alexander, Bradley T. Christian
Summary: The study focused on the correlation between white matter microstructure and amyloid load in adults with DS at risk for developing AD. Results indicated widespread age-by-amyloid interaction, with negative association of FA and positive association of MD with amyloid. These findings align with white matter microstructural changes observed in late onset AD in non-DS populations.
NEUROIMAGE-CLINICAL
(2022)
Article
Biochemistry & Molecular Biology
Silvia De Caro, Giulia De Soricellis, Simone Dell'Acqua, Enrico Monzani, Stefania Nicolis
Summary: Both beta-amyloid peptides and oxidative stress are important factors in Alzheimer's disease. Hemin, which has redox properties, contributes to the disease's development and its level increases in pathological conditions and traumatic brain injuries. This study aimed to investigate the reactivity of the hemin-beta-amyloid(16) complex and found that it can catalyze oxidation and nitration reactions. The results showed that the complex binds negatively charged substrates with higher affinity and the tyrosine residue is the target of nitration. The study also found that hemin degradation is partly prevented by the coordinated peptide.
Article
Neurosciences
Eleanor Drummond, Tomas Kavanagh, Geoffrey Pires, Mitchell Marta-Ariza, Evgeny Kanshin, Shruti Nayak, Arline Faustin, Valentin Berdah, Beatrix Ueberheide, Thomas Wisniewski
Summary: This study comprehensively identified proteins that are enriched in amyloid plaques using unbiased proteomics in two subtypes of early onset AD: sporadic early onset AD (EOAD) and Down Syndrome (DS) with AD. The study found that many proteins were consistently enriched in amyloid plaques compared to beta amyloid (A beta), with endosomal/lysosomal proteins particularly highly enriched. The study also showed that the amount of enrichment of some proteins differed between EOAD and DS. These findings suggest that these enriched proteins could serve as potential therapeutic targets and/or biomarkers for AD.
ACTA NEUROPATHOLOGICA COMMUNICATIONS
(2022)
Article
Biochemistry & Molecular Biology
Shojiro Ichimata, Ivan Martinez-Valbuena, Seojin Lee, Jun Li, Ali M. Karakani, Gabor G. Kovacs
Summary: Limited comparative data exist on the molecular spectrum of amyloid-beta (Aβ) and tau deposition in individuals with Down syndrome (DS) and sporadic Alzheimer's disease (sAD). We found that DS cases had more severe Aβ and tau deposition in the temporal lobe and cerebellum compared to sAD cases, as confirmed by both semi-quantitative and quantitative analysis.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Neurosciences
Shiveena Bhatia, Rishi Rawal, Pratibha Sharma, Tanveer Singh, Manjinder Singh, Varinder Singh
Summary: Alzheimer's disease is a major cause of senile dementia, characterized by accumulation of plaques and tangles in the brain leading to neurodegeneration and cell death, along with other pathological features such as abnormal microvasculature and increased beta-amyloid production. Mitochondrial Dysfunction (MD) is implicated in all associated AD pathologies, with evidence suggesting its involvement in the progression of neurodegeneration in AD.
CURRENT NEUROPHARMACOLOGY
(2022)
Article
Neurosciences
Aimee N. Winter, Erika K. Ross, Heather M. Wilkins, Trisha R. Stankiewicz, Tyler Wallace, Keith Miller, Daniel A. Linseman
NUTRITIONAL NEUROSCIENCE
(2018)
Review
Geriatrics & Gerontology
Tina E. Brinkley, Miles Berger, Kathryn E. Callahan, Robert A. Fieo, Lee A. Jennings, Jill K. Morris, Heather M. Wilkins, Stephen B. Kritchevsky
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
(2018)
Correction
Geriatrics & Gerontology
Tina E. Brinkley, Miles Berger, Kathryn E. Callahan, Robert A. Fieo, Lee A. Jennings, Jill K. Morris, Heather M. Wilkins, Stephen B. Kritchevsky
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
(2019)
Article
Clinical Neurology
Jeffrey M. Statland, Dan Moore, Yunxia Wang, Maureen Walsh, Tahseen Mozaffar, Lauren Elman, Sharon P. Nations, Hiroshi Mitsumoto, J. Americo Fernandes, David Saperstein, Ghazala Hayat, Laura Herbelin, Chafic Karam, Jonathan Katz, Heather M. Wilkins, Abdulbaki Agbas, Russell H. Swerdlow, Regina M. Santella, Mazen M. Dimachkie, Richard J. Barohn
Article
Neurosciences
Yan Ji, Xiaowan Wang, Colin Kalicki, Blaise W. Menta, Megan Baumgardner, Scott J. Koppel, Ian W. Weidling, Judit Perez-Ortiz, Heather M. Wilkins, Russell H. Swerdlow
JOURNAL OF ALZHEIMERS DISEASE
(2019)
Article
Neurosciences
Kristin Marquardt, Megan Josey, Johnny A. Kenton, James F. Cavanagh, Andrew Holmes, Jonathan L. Brigman
Article
Neurosciences
Amber Watts, Heather M. Wilkins, Elias Michaelis, Russell H. Swerdlow
JOURNAL OF ALZHEIMERS DISEASE
(2019)
Article
Neurosciences
Kristin Marquardt, James F. Cavanagh, Jonathan L. Brigman
Review
Biochemistry & Molecular Biology
Natalie S. Swerdlow, Heather M. Wilkins
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2020)
Article
Cell Biology
Heather M. Wilkins, Xiaowan Wang, Blaise W. Menta, Scott J. Koppel, Rebecca Bothwell, Annette M. Becker, Heidi Anderson, Erin Schwartz, Dong Pei, Nanda K. Yellapu, Prabhakar Chalise, Cynthia M. Gouvion, Mohammad Haeri, Jeffrey M. Burns, Russell H. Swerdlow
Summary: The study revealed that the APOE ε4 genotype affects platelet and lymphocyte metabolism in Alzheimer's disease patients, showing lower platelet mitochondrial activity and higher lymphocyte apoptosis markers in APOE ε4 carriers. Proteins related to mitophagy and energy sensing were elevated in APOE ε4 lymphocytes, possibly representing compensatory changes. RNA sequencing also indicated activation of inflammatory pathways and modulation of bioenergetic signaling in APOE ε4 carriers.
Review
Pharmacology & Pharmacy
Benjamin R. Troutwine, Laylan Hamid, Colton R. Lysaker, Taylor A. Strope, Heather M. Wilkins
Summary: Genetic variation in the APOE gene is associated with the risk of Alzheimer's disease. The APOE epsilon 4 alleles are the strongest genetic risk factor for late onset sporadic AD, while the APOE epsilon 2 alleles have lower risk and the APOE epsilon 3 alleles have neutral risk.
ACTA PHARMACEUTICA SINICA B
(2022)
Review
Biochemistry & Molecular Biology
Taylor A. Strope, Cole J. Birky, Heather M. Wilkins
Summary: Mitochondrial and bioenergetic dysfunction is a common feature in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Mitochondria play a crucial role in controlling cellular processes and may drive the pathological changes in these diseases.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Heather M. Wilkins
Summary: Mitochondrial dysfunction and Aβ accumulation are characteristic features of Alzheimer's disease. Previous research suggests a relationship between the protein APP and Aβ with mitochondrial function, and that changes in mitochondrial function can affect the production of Aβ from APP. The role of these interactions in AD pathology and progression remains unclear. This article discusses the reliability of prior studies and the critical gaps in knowledge regarding the relationships between APP, Aβ, and mitochondria.
BIOCHEMICAL SOCIETY TRANSACTIONS
(2023)
Article
Neurosciences
Taylor A. Strope, Heather M. Wilkins
Summary: Processing of Amyloid Precursor Protein (APP) to amyloid beta (Ab) is a key characteristic of Alzheimer's disease (AD). The accumulation and aggregation of Ab is believed to cause AD, but recent attempts to target Ab therapeutically have been unsuccessful. Research has also evidenced metabolic deficits and mitochondrial dysfunction in AD, with localization of APP and γ-secretase to mitochondria. This article explores the evidence of the mitochondrial localization of APP and γ-secretase, and discusses their implications in regulating mitochondrial function.
CURRENT OPINION IN NEUROBIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Daniel A. Linseman, Aimee N. Winter, Heather M. Wilkins
Summary: Mitochondrial oxidative stress and dysfunction play a significant role in the pathogenesis of ALS. The G93A mutant SOD1 disrupts mitochondrial GSH uptake and reduces the binding of GSH to Bcl-2 protein. In the ALS mouse model, mitochondrial GSH is depleted in the spinal cord, and this depletion is associated with the S-nitrosylation of the OGC protein and disruption of the Bcl-2/GSH interaction.