Exposure of Mesenchymal Stem Cells to an Alzheimer’s Disease Environment Enhances Therapeutic Effects by Sang Eon Park, Hyeong Seop Kim, Soo Jin Kwon, Min-Jeong Kim, Suk-joo Choi, Soo-young Oh, Gyu Ha Ryu, Hong Bae Jeon, Duk L. Na, Jong Wook Chang

“…Previous studies suggested that the coculture of human MSCs with AD in an in vitro model reduced the expression of amyloid-beta 42 (Aβ42) in the medium as well as the overexpression of amyloid-beta- (Aβ-) degrading enzymes such as neprilysin (NEP). …”
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Blood biomarkers for vascular cognitive impairment based on neuronal function: a systematic review and meta-analysis by Weiquan Huang, Libin Liao, Qian Liu, Rongchao Ma, Xuan He, Xuan He, Xiaoqiong Du, Dujuan Sha, Dujuan Sha, Dujuan Sha, Dujuan Sha

“…The nine peripheral biomarkers analyzed for their association with neuronal function include amyloid beta 42 (Aβ42), amyloid beta 40 (Aβ40), Aβ42/Aβ40 ratio, total Tau (t-Tau), phosphorylated tau 181 (p-tau 181), neurofilament light (NfL), brain-derived neurotrophic factor (BDNF), S100B, and soluble receptor for advanced glycation end products (sRAGE). …”
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Elevation of ganglioside degradation pathway drives GM2 and GM3 within amyloid plaques in a transgenic mouse model of Alzheimer's disease by Wenxuan Wang, Sarah J. Myers, Nikita Ollen-Bittle, Shawn N. Whitehead

“…Ganglioside dysregulation has been implicated in various neurodegenerative diseases, including AD, but the spatial distribution of ganglioside dysregulation with respect to amyloid-beta (Aβ) deposition is not well understood. …”
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Investigation of Novel Aronia Bioactive Fraction-Alginic Acid Nanocomplex on the Enhanced Modulation of Neuroinflammation and Inhibition of Aβ Aggregation by Bong-Keun Jang, Soo Jung Shin, Hyun Ha Park, Vijay Kumar, Yong Ho Park, Jeom-Yong Kim, Hye-Yeon Kang, Sunyoung Park, Youngsun Kwon, Sang-Eun Shin, Minho Moon, Beom-Jin Lee

“…Background/Objectives: Aronia extract or its active compounds, especially anthocyanin, have shown potential for Alzheimer’s disease (AD)-related pathologies, including neuroinflammation, fibrillogenesis of amyloid beta (Aβ), and cognitive impairment. However, there was still concern about their structural instability in vivo and in vitro. …”
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Down but Not Out: The Consequences of Pretangle Tau in the Locus Coeruleus by Termpanit Chalermpalanupap, David Weinshenker, Jacki M. Rorabaugh

“…The LC is the main source of norepinephrine (NE) in the forebrain, and its degeneration is highly correlated with cognitive impairment and amyloid-beta (Aβ) and tangle pathology. Hyperphosphorylated tau in the LC is among the first detectable AD-like neuropathology in the brain, and while the LC/NE system impacts multiple aspects of AD (e.g., cognition, neuropathology, and neuroinflammation), the functional consequences of hyperphosphorylated tau accrual on LC neurons are not known. …”
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Mitochondrial dysfunction in Alzheimer’s disease: a key frontier for future targeted therapies by Shuguang Wang, Zuning Liao, Qiying Zhang, Xinyuan Han, Changqing Liu, Jin Wang

“…These mitochondrial abnormalities are closely associated with amyloid-beta and tau protein pathology, collectively accelerating the neurodegenerative process. …”
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Lipidome disruption in Alzheimer’s disease brain: detection, pathological mechanisms, and therapeutic implications by Sijia He, Ziying Xu, Xianlin Han

“…To elucidate the central role of lipids in converging multiple pathological aspects of AD, we reviewed the current knowledge on the interplay between lipids and major AD features, including amyloid beta, tau, and neuroinflammation. Finally, we assessed the progresses and obstacles in lipid-based therapeutics and proposed potential strategies for leveraging lipidomics in the treatment of AD.…”
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Interplay of p23 with FKBP51 and their chaperone complex in regulating tau aggregation by Pijush Chakraborty, Markus Zweckstetter

“…Abstract The pathological deposition of tau and amyloid-beta into insoluble amyloid fibrils are pathological hallmarks of Alzheimer’s disease. …”
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Therapeutic Actions of the Thiazolidinediones in Alzheimer’s Disease by María José Pérez, Rodrigo A. Quintanilla

“…In the AD brain is common to observe the accumulation of senile plaques formed by amyloid-beta (Aβ) peptide and the neurofibrillary tangles composed of modified tau protein, which both lead to cellular damage and progressive neurodegeneration. …”
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Spines, Plasticity, and Cognition in Alzheimer's Model Mice by Tara Spires-Jones, Shira Knafo

“…The pathological hallmarks of Alzheimer's disease (AD)—widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles—have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. …”
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The Science of Memory Loss: Insights into Alzheimer’s Disease by Agnieszka Starzyk, Piotr Charzewski

“…Emerging therapies, such as monoclonal antibodies targeting amyloid-beta and tau proteins, show promise but are hindered by challenges in efficacy and safety. …”
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How close is autophagy-targeting therapy for Alzheimer's disease to clinical use? A summary of autophagy modulators in clinical studies by Sofia Miranda Fernandes, Johanna Mayer, Per Nilsson, Makoto Shimozawa

“…A pathological hallmark of AD is the accumulation of aberrant protein/peptide aggregates such as extracellular amyloid plaques containing amyloid-beta peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. …”
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Navigating the Role and Approach of Gut Microbiota in Addressing Alzheimer's Disease Pathogenesis by Imrana Jazuli, Akeela Jazeel, Lakshmi Selvaratnam, Deepa Alex, Yatinesh Kumari

“… Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid beta plaques and tau protein neurofibrillary tangles, leading to cognitive decline. …”
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Circuitry and Synaptic Dysfunction in Alzheimer’s Disease: A New Tau Hypothesis by Siddhartha Mondragón-Rodríguez, Humberto Salgado-Burgos, Fernando Peña-Ortega

“…For more than five decades, the field of Alzheimer’s disease (AD) has focused on two main hypotheses positing amyloid-beta (Aβ) and Tau phosphorylation (pTau) as key pathogenic mediators. …”
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Musical Electroacupuncture May Be a Better Choice than Electroacupuncture in a Mouse Model of Alzheimer’s Disease by Jing Jiang, Gang Liu, Suhua Shi, Zhigang Li

“…Moreover, MEA therapy performed better than EA treatment in decreasing amyloid-beta levels in the frontal lobe of mice with AD. …”
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Activation of Macrophages by Oligomeric Proteins of Different Size and Origin by Indrė Dalgėdienė, Asta Lučiūnaitė, Aurelija Žvirblienė

“…Our aim was to investigate the phenotype of macrophages after activation with different oligomeric proteins and their IC. We have used amyloid beta (Aβ1–42) that plays a role in neurodegenerative inflammation as a model of host-associated protein and three oligomeric viral antigens as pathogen-associated proteins. …”
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Sudden Intrabulbar Amyloid Increase Simultaneously Disrupts Olfactory Bulb Oscillations and Odor Detection by Rebeca Hernández-Soto, Keila Dara Rojas-García, Fernando Peña-Ortega

“…There seems to be a correlation between soluble amyloid beta protein (Aβ) accumulation in the main olfactory bulb (OB) and smell deterioration in both Alzheimer’s disease (AD) patients and animal models. …”
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On the Environmental Factors Affecting the Structural and Cytotoxic Properties of IAPP Peptides by Marianna Flora Tomasello, Alessandro Sinopoli, Giuseppe Pappalardo

“…Current theories proposed for the mechanisms of toxicity will be also summarized together with an outline of the underlying molecular links between IAPP and amyloid beta (Aβ) misfolding.…”
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Longitudinal characterization reveals behavioral impairments in aged APP knock in mouse models by Lisa Blackmer-Raynolds, Lyndsey D. Lipson, Isabel Fraccaroli, Ian N. Krout, Jianjun Chang, Timothy Robert Sampson

“…Abstract APP knock-in (KI) mice serve as an exciting new model system to understand amyloid beta (Aβ) pathology, overcoming many of the limitations of previous overexpression-based model systems. …”
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Unveiling FOXO3's metabolic contribution to menopause and Alzheimer's disease by Christopher O'Mahony, Oscar Hidalgo-Lanussa, George E. Barreto

“…Neurometabolic alterations during the endocrine transition emerge as early indicators of AD pathology, including reduced glucose metabolism and increased amyloid-beta (Aβ) deposition. The fluctuating endocrine environment, marked by declining estradiol levels and reduced estrogen receptor beta (ERβ) activity, further exacerbates this process. …”
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