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Biochemistry & Molecular Biology
Saffire H. Krance et al.
Summary: The study found that concentrations of clusterin and complement component 3 were significantly higher in the cerebrospinal fluid of Alzheimer's disease patients, while C-reactive protein concentrations were elevated in peripheral blood. The results collectively support elevated complement pathway activity in AD, characterized by increased CSF clusterin concentrations and inconsistently reflected by peripheral blood proteins related to an AD diagnosis.
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Summary: The study found that miR-298 may have potential therapeutic effects on Alzheimer's disease by inhibiting the expression of key proteins and influencing posttranslational levels of tau protein. This research opens up new possibilities for miR-298 to become a target for Alzheimer's disease therapy.
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Summary: The decrease in circulating adiponectin levels is associated with neurodegeneration, neuroinflammation, and Alzheimer's disease pathologies. Increasing adiponectin through treatments like adipoRon can improve neuronal insulin signaling, memory functions, and reduce amyloid levels in Alzheimer's disease models.
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Summary: Traumatic brain injury is a risk factor for neurodegenerative diseases, particularly chronic traumatic encephalopathy. This study identified biomarker signatures associated with chronic anxiety traits and behavioral, cognitive, and memory complaints in individuals exposed to blast injuries.
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Joseph Therriault et al.
Summary: Through analysis of three independent samples of cognitively unimpaired, mild cognitive impairment, and Alzheimer's disease subjects, the study found that the interaction effect between APOE epsilon 4 and amyloid-beta was related to increased tau load in Alzheimer's disease-vulnerable regions. The interaction between one APOE epsilon 4 allele and amyloid-beta led to increased tau load, while the interaction between amyloid-beta and two APOE epsilon 4 alleles was associated with a more widespread pattern of tau aggregation.
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May A. Beydoun et al.
Summary: The study suggests that co-infection between Helicobacter pylori and specific periodontal pathogens may alter the onset of Alzheimer's disease and all-cause dementia. Certain periodontal pathogens interact synergistically or antagonistically with Hp sero-positivity, affecting the risk of both types of dementia.
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Yin Xu et al.
Summary: The transcription factor EB (TFEB) plays a crucial role in the lysosomal exocytosis of selected tau species, with TFEB loss causing a decrease in tau levels and accelerated spreading within neurons. This suggests that TFEB-mediated tau exocytosis acts as a clearance mechanism to reduce intracellular tau levels under pathological conditions.
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Anne Nitsche et al.
Summary: Alzheimer's disease is a neurodegenerative disorder that predominantly affects elderly humans, with little occurrence in non-primate mammals and non-human primates. Research shows that most AD-associated genes have ancient evolutionary origins, but exhibit faster gene structure evolution in loci with AD-related expression changes. Particularly, non-coding genes associated with AD play a significant role in the disease.
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H. Stocker et al.
Summary: The study found that the AD polygenic risk score (PRS) and APOE status could effectively predict the clinical diagnosis of AD, VD, MD, and all-cause dementia in a community-based cohort.
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Daniela Monteiro-Fernandes et al.
Summary: Despite progress in understanding AD neuropathology, there is no effective treatment for the memory deficits caused by A beta and Tau protein accumulation. However, positive allosteric modulation of AMPA receptors shows promise in restoring memory and synaptic signaling in non-transgenic animal models.
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Swagata Ghatak et al.
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Laetitia Lemoine et al.
Summary: This study demonstrates differences in the properties of amyloid plaques between two genetic variants of AD and sAD. Despite the lack of measurable amyloid fibrils in AβPP mutation carriers, high regional tau and astrocyte binding were observed. Differences in the pathological cascade between AD variants were suggested, warranting further exploration in vivo.
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Summary: The study reveals that aberrantly activated anaplastic lymphoma kinase (ALK) is a key factor contributing to the pathology of Alzheimer's disease (AD), by inducing abnormal accumulation of tau protein and causing dysfunction in neurons. The research demonstrates that ALK disrupts autophagosome maturation, leading to tau accumulation and aggregation, ultimately resulting in neuronal dysfunction in AD.
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Marco Bucci et al.
Summary: It is important to find biomarkers for early detection of Alzheimer's disease. This study compared cerebrospinal fluid and imaging biomarkers to predict cognitive decline in Alzheimer's patients. The results showed that PET tau was superior to CSF p-Tau181 and PET amyloid-beta in predicting cognitive decline.
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Biochemistry & Molecular Biology
H. Stocker et al.
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Matias Wagner et al.
Summary: Frontotemporal dementia (FTD) is a clinically and genetically heterogeneous disorder. A study involving 509 FTD patients in Germany identified pathogenic variants in genes such as C9orf72, GRN, and MAPT. TBK1-associated FTD was found to be relatively common, and a homozygous missense variant in CTSF was confirmed as a new FTD gene.
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Andrew G. B. Thompson et al.
Summary: Plasma tau and NfL show potential as biomarkers for prion disease, with diagnostic value in distinguishing disease types and clinical relevance in disease progression. In asymptomatic PRNP mutation carriers, plasma NfL levels start to rise years before symptom onset, indicating potential as a marker for disease onset.
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Nicholas Brookhouser et al.
Summary: The study revealed that the APOE2 variant reduces the risk of developing Alzheimer's disease and showed that converting APOE3 to APOE2 significantly decreased the production of amyloid-beta peptides. Furthermore, it was demonstrated that the protective effects of APOE2 may be related to a mechanism involving non-amyloidogenic processing.
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Ding-Yuan Tian et al.
Summary: This study investigated the impact of unilateral nephrectomy on Aβ clearance in both humans and animals, finding that the kidney plays a physiological role in clearing Aβ. Furthermore, chronic furosemide treatment was shown to reduce Aβ levels in the blood and brain, attenuate AD pathologies, and improve cognitive deficits in APP/PS1 mice. These findings suggest that facilitation of Aβ clearance via the kidney could be a novel potential therapeutic approach for AD.
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Woo-In Ryu et al.
Summary: The study found that neural progenitor cells and astrocytes differentiated from induced pluripotent stem cells of late-onset Alzheimer's disease patients exhibit multiple inter-related bioenergetic alterations, including changes in mitochondrial respiration, reduced levels of NAD/NADH, and diminished glucose uptake. These findings suggest that Alzheimer's disease may involve multiple hits and innate inefficient cellular energy management.
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Amit Kumar et al.
Summary: The study demonstrates that the novel astrocytic PET ligand BU99008 can visualize reactive astrogliosis in postmortem AD brains and proposes a multiple binding site model for different ligands in AD and control brains. The data shows significant differences in the proportion and affinities of binding sites between AD and control groups, indicating potential targets for future research.
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Michael Wainberg et al.
Summary: Recent studies have reignited interest in the hypothesis that infectious agents, particularly herpesviruses, may contribute to Alzheimer's disease pathogenesis. These studies suggest that many key features of Alzheimer's disease, like amyloid beta production and neuroinflammation, may actually be protective responses to acute infection that become maladaptive in the case of chronic infection.
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Biochemistry & Molecular Biology
Rodrigo Morales et al.
Summary: This study demonstrates that administration of Aβ seeds through various peripheral routes can accelerate the accumulation of Aβ in the brains of AD mouse models. Oral administration of brain extracts had no impact on brain pathology. The peripheral administration of Aβ seeds led to the generation of a large proportion of aggregates in blood vessels, suggesting a role of vascular transport in AD-related pathological changes.
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Biochemistry & Molecular Biology
Andrew Tsatsanis et al.
Summary: Amyloidogenic processing of the amyloid precursor protein leads to the formation of amyloid-beta peptide plaques in Alzheimer's disease. Early cortical changes in AD also involve neuroinflammation and elevated iron levels. The activation of the innate immune system in the brain is a neuroprotective response to infection, but persistent neuroinflammation is linked to AD neuropathology through unknown mechanisms.
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Rebecca Panitch et al.
Summary: The study found that the protective effect of APOE ε2 against Alzheimer's disease may be related to the complement pathway, involving genes such as C4A, C4B, and HSPA2. An AD-specific co-expression network was identified in APOE ε2/ε3 carriers, primarily associated with tau pathology.
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Editorial Material
Biochemistry & Molecular Biology
Zhangying Chen et al.
Summary: The three-dimensional graphic design illustrates the potential role of meningeal vessels in Alzheimer disease, showing the clearance of solutes from meningeal lymphatic vessels. The image highlights differences between APOE4(+) and APOE4(-) Alzheimer disease cases outlined in the accompanying Comment article.
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Luis Enrique Arroyo-Garcia et al.
Summary: The study found a significant degradation in gamma oscillation power in the App(NL-G-F) mouse model, independent of and preceding amyloid plaque formation and cognitive impairment reported previously. This degradation is correlated with increased concentration of A beta(1-42) in the brain.
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Ya-Nan Ou et al.
Summary: The study identified 7 brain proteins as causal in Alzheimer's disease, with ACE and SNX32 also being associated with AD at the blood transcriptomic level. These findings may provide important leads for future functional studies and potential drug targets for AD.
MOLECULAR PSYCHIATRY
(2021)
Correction
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Zhangying Chen et al.
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Sujeong Yang et al.
Summary: Perineuronal nets (PNNs), containing chondroitin sulphate proteoglycans on neuronal surfaces, play a role in neuroplasticity and memory. Age-related reduction of chondroitin 6-sulphates (C6S) in PNNs leads to increased inhibition. Manipulating CS composition of PNNs can restore neuroplasticity and memory deficits in aged mice, with a focus on the importance of C6S in memory and neuroplasticity.
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Valeria Calsolaro et al.
Summary: This study utilized a novel PET tracer, C-11-BU99008, to investigate astrocyte reactivity associated with Alzheimer's disease, revealing significantly increased astrocyte reactivity in older cognitively impaired and Alzheimer's disease patients, particularly in cortical regions.
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Mary Ann A. DeMichele-Sweet et al.
Summary: Psychotic symptoms in Alzheimer's disease are common and have genetic components, with significant associations found in two loci - ENPP6 and SUMF1. AD + P shows negative genetic correlations with cognitive and educational attainment, and positive genetic correlations with depressive symptoms. This study provides insights into the genetic architecture of psychosis in Alzheimer's disease.
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Review
Biochemistry & Molecular Biology
Harald Hampel et al.
Summary: Breakthroughs in molecular medicine have highlighted the significance of the amyloid-beta pathway in the pathophysiology of Alzheimer's disease. Established biochemical alterations of the A beta cycle serve as promising targets for the development of disease-modifying therapies. Research indicates a crucial role of A beta pathway dyshomeostasis in the dynamics of AD pathophysiology, supporting the development of A beta-targeting therapeutic strategies for early treatment of AD.
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Fanny Eysert et al.
Summary: Research has shown that FERMT2 plays an important regulatory role in APP metabolism, and underexpression of FERMT2 can affect axonal growth, synaptic connectivity, and long-term potentiation, which may impact the pathogenesis of Alzheimer's disease (AD).
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