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Converging links between adult-onset neurodegenerative Alzheimer’s disease and early life neurodegenerative neuronal ceroid lipofuscinosis?

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Neural Regeneration Research 2023年第7期18卷 1463-1471页

作者： Marcel Klein Guido Hermey Institute for molecular and Cellular Cognition Center for Molecular Neurobiology HamburgUniversity Medical Center Hamburg-EppendorfHamburgGermany

Evidence from genetics and from analyzing cellular and animal models have converged to suggest links between neurodegenerative disorders of early and late ***,we summarize emerging links between the most common late life neurodegenerative disease,Alzheimer’s disease,and the most common early life neurodegenerative diseases,neuronal ceroid *** studies reported an overlap of clinically diagnosed Alzheimer’s disease and mutations in genes known to cause neuronal ceroid *** data strongly suggest dysfunction of intracellular trafficking mechanisms and the autophagy-endolysosome system in both types of neurodegenerative *** suggests shared cytopathological processes underlying these different types of neurodegenerative diseases.A better understanding of the common mechanisms underlying the different diseases is important as this might lead to the identification of novel targets for therapeutic concepts,the transfer of therapeutic strategies from one disease to the other and therapeutic approaches tailored to patients with specific ***,we review dysfunctions of the endolysosomal autophagy pathway in Alzheimer’s disease and neuronal ceroid lipofuscinoses and summarize emerging etiologic and genetic overlaps.

关键词： Alzheimer’s disease autophagy Batten disease CLN3 disease dementia endosome lysosome neurodegeneration neuronal ceroid lipofuscinosis presenilin

Deciphering the transcriptomic signature of synaptic activity

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Neural Regeneration Research 2022年第1期17卷 82-84页

作者： Guido Hermey Institute for molecular and Cellular Cognition Center for Molecular Neurobiology HamburgUniversity Medical Center Hamburg-EppendorfHamburgGermany

Neurons undergo activity-dependent changes in their molecular composition and structure in order to regulate cellular processes such as dendritic growth,synapse elimination,spine maturation and synaptic *** synaptic plasticity plays an important role during a critical period in brain development and contributes to sensory adaptation and to learning and memory in the mature nervous *** dysregulation underlies a number of pathological processes in psychiatric and neurodegenerative disorders,such as addiction.

关键词： strength. signature elimination

Intracellular sorting pathways of the amyloid precursor protein provide novel neuroprotective strategies

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Neural Regeneration Research 2015年第11期10卷 1727-1728页

作者： Guido Hermey Institute for molecular and Cellular Cognition Center for Molecular Neurobiology Hamburg University Medical Center Hamburg-Eppendorf

Alzheimer＇s disease（AD）is the most common cause of senile *** is characterized by the formation of plaques mainly composed of the amyloid-beta peptide（Aβ）.Diverse lines of evidence support the notion that accumulation of Aβis a primary cause of AD pathogenesis（Huang and Mucke,2012）.Amyloid precusor protein（APP）processing is dependent on its subcelluar trafficking pathway：Aβis derived from APP by proteolyric processing.

关键词： APP Intracellular sorting pathways of the amyloid precursor protein provide novel neuroprotective strategies CS

Olfactory receptors in neural regeneration in the central nervous system

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Neural Regeneration Research 2025年第9期20卷 2480-2494页

作者： Rafael Franco Claudia Garrigós Toni Capó Joan Serrano-Marín Rafael Rivas-Santisteban Jaume Lillo molecular neurobiology Laboratory Department of Biochemistry and Molecular BiomedicineFacultat de BiologiaUniversitat de BarcelonaBarcelonaSpain CiberNed Network center for Biomedical Research in Neurodegenerative Diseases Spanish National Health Institute Carlos ⅢMadridSpain School of Chemistry Universitat de BarcelonaBarcelonaSpain Department of Biochemistry and Physiology School of Pharmacy and Food SciencesUniversitat de BarcelonaBarcelonaSpain Laboratory of Computational Medicine Biostatistics UnitFaculty of MedicineAutonomous University of BarcelonaCampus BellaterraBarcelonaSpain

Olfactory receptors are crucial for detecting odors and play a vital role in our sense of smell,influencing behaviors from food choices to emotional *** receptors also contribute to our perception of flavor and have potential applications in medical diagnostics and environmental *** ability of the olfactory system to regenerate its sensory neurons provides a unique model to study neural regeneration,a phenomenon largely absent in the central nervous *** gained from how olfactory neurons continuously replace themselves and reestablish functional connections can provide strategies to promote similar regenerative processes in the central nervous system,where damage often results in permanent *** the molecular and cellular mechanisms underpinning olfactory neuron regeneration could pave the way for developing therapeutic approaches to treat spinal co rd injuries and neurodegenerative diseases like Alzheimer's *** ctory receptors are found in almost any cell of eve ry orga n/tissue of the mammalian *** ectopic expression provides insights into the chemical structures that can activate olfactory *** addition to odors,olfactory receptors in ectopic expression may respond to endogenous compounds and molecules produced by mucosal colonizing *** analysis of the function of olfactory receptors in ectopic expression provides valuable information on the signaling pathway engaged upon receptor activation and the receptor's role in proliferation and cell differentiation *** review explo res the ectopic expression of olfa ctory receptors and the role they may play in neural regeneration within the central nervous system,with particular attention to compounds that can activate these receptors to initiate regenerative *** suggests that olfactory receptors could serve as potential therapeutic targets for enhancing neural repair and recovery following central nervous syste

关键词： adenosine receptors adrenergic receptors ectopic expression G proteincoupled receptors glia neurons

SYNGR4 and PLEKHB1 deregulation in motor neurons of amyotrophic lateral sclerosis models: potential contributions to pathobiology

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Neural Regeneration Research 2022年第2期17卷 266-270页

作者： Rita F.Marques Kent E.Duncan Institute for Biochemistry and molecular Biology Department of ChemistryUniversity of HamburgHamburgGermany Neuronal Translational Control Research Group Center for Molecular Neurobiology Hamburg(ZMNH)University Medical Center Hamburg-EppendorfHamburgGermany

Amyotrophic lateral sclerosis is the most common adult-onset neurodegenerative disease affecting motor neurons. Its defining feature is progressive loss of motor neuron function in the cortex, brainstem, and spinal cord, leading to paralysis and death. Despite major advances in identifying genes that can cause disease when mutated and model the disease in animals and cellular models, it still remains unclear why motor symptoms suddenly appear after a long pre-symptomatic phase of apparently normal function. One hypothesis is that age-related deregulation of specific proteins within key cell types, especially motor neurons themselves, initiates disease symptom appearance and may also drive progressive degeneration. Genome-wide in vivo cell-type-specific screening tools are enabling identification of candidates for such proteins. In this minireview, we first briefly discuss the methodology used in a recent study that applied a motor neuron-specific RNASeq screening approach to a standard model of TAR DNA-binding protein-43(TDP-43)-driven amyotrophic lateral sclerosis. A key finding of this study is that synaptogyrin-4 and pleckstrin homology domain-containing family B member 1 are also deregulated at the protein level within motor neurons of two unrelated mouse models of mutant TDP-43 driven amyotrophic lateral sclerosis. Guided by what is known about molecular and cellular functions of these proteins and their orthologs, we outline here specific hypotheses for how changes in their levels might potentially alter cellular physiology of motor neurons and detrimentally affect motor neuron function. Where possible, we also discuss how this information could potentially be used in a translational context to develop new therapeutic strategies for this currently incurable, devastating disease.

关键词： amyotrophic lateral sclerosis glucagon-like peptide-1 receptor motor neuron disease mouse model neurodegeneration phosphatidylserine pleckstrin homology domain synaptogyrin TAR DNA-binding protein-43 vesicle transport

Potential role of tanycyte-derived neurogenesis in Alzheimer's disease

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Neural Regeneration Research 2025年第6期20卷 1599-1612页

作者： Guibo Qi Han Tang Jianian Hu Siying Kang Song Qin Department of Anatomy Histologyand EmbryologySchool of Basic Medical SciencesFudan UniversityShanghaiChina State Key Laboratory of Medical neurobiology and MOE Frontiers center for Brain Science Fudan UniversityShanghaiChina

Tanycytes, specialized ependymal cells located in the hypothalamus, play a crucial role in the generation of new neurons that contribute to the neural circuits responsible for regulating the systemic energy balance. The precise coordination of the gene networks controlling neurogenesis in naive and mature tanycytes is essential for maintaining homeostasis in adulthood. However, our understanding of the molecular mechanisms and signaling pathways that govern the proliferation and differentiation of tanycytes into neurons remains limited. This article aims to review the recent advancements in research into the mechanisms and functions of tanycyte-derived neurogenesis. Studies employing lineage-tracing techniques have revealed that the neurogenesis specifically originating from tanycytes in the hypothalamus has a compensatory role in neuronal loss and helps maintain energy homeostasis during metabolic diseases. Intriguingly,metabolic disorders are considered early biomarkers of Alzheimer's disease. Furthermore,the neurogenic potential of tanycytes and the state of newborn neurons derived from tanycytes heavily depend on the maintenance of mild microenvironments, which may be disrupted in Alzheimer's disease due to the impaired blood–brain barrier ***, the specific alterations and regulatory mechanisms governing tanycyte-derived neurogenesis in Alzheimer's disease remain unclear. Accumulating evidence suggests that tanycyte-derived neurogenesis might be impaired in Alzheimer's disease, exacerbating neurodegeneration. Confirming this hypothesis, however, poses a challenge because of the lack of long-term tracing and nucleus-specific analyses of newborn neurons in the hypothalamus of patients with Alzheimer's disease. Further research into the molecular mechanisms underlying tanycyte-derived neurogenesis holds promise for identifying small molecules capable of restoring tanycyte proliferation in neurodegenerative diseases. This line of investigation could pro

关键词： Alzheimer's disease blood–brain barrier ependymoglial cells hypothalamus metabolic diseases neural stem cells neurogenesis neuroinflammatory diseases neurons tanycyte

The neuroprotective and regenerative potential of parkin and GDNF/Ret signaling in the midbrain dopaminergic system

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Neural Regeneration Research 2015年第11期10卷 1752-1753页

作者： Edgar R.Kramer Development and Maintenance of the Nervous System Center for Molecular Neurobiology University Medical Center Hamburg-Eppendorf

Parkinson＇s disease（PD）is the second most common neurodegenerative disease after Alzheimer＇s *** etiology of PD is still not completely understood,but the degeneration of dopaminergic（DA）neurons in the substantia nigra pars compacta（SNpc）,loss of DA innervation of the striatum,and protein aggregates in the form of Lewy bodies and neurites are its established hallmarks. In addition to α-synuclein accumu- lation in Lewy bodies and neurites, genetic mutations in the genes encoding parkin, PINK, DJ-1, LRRK2 and other proteins are associated with the inherited form of PD. An association study linked also the receptor tyrosine kinase Ret to PD （Meka et al., 2015）. Currently there are only symptomatic treatments available for PD but no cure. Consequently much effort is being made to find neurotrophic and other factors able to stimulate SNpc DA neuron protection and regeneration.

关键词： GDNF The neuroprotective and regenerative potential of parkin and GDNF/Ret signaling in the midbrain dopaminergic system

L1 is a potential marker for poorly-differentiated pancreatic neuroendocrine carcinoma

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World Journal of Gastroenterology 2006年第1期12卷 94-98页

作者： Jussuf T Kaifi Ulrich Zinnkann Emre F Yekebas Paulus G Schurr Uta Reichelt Robin Wachowiak Henning C Fiegel Susann Petri Melitta Schachner Jakob RIzbicki Department of General Visceral and Thoracic SurgeryUniversity Medical Center Hamburg-EppendorfHamburgGermany Institute for Pathology University Medical Center Hamburg-EppendorfHamburgGermany Department of Pediatric Surgery University Medical Center Hamburg-EppendorfHamburgGermany center for molecular neurobiology University Medical Center Hamburg-EppendorfHamburgGermany

AIM： To determine the expression of L1 in pancreatic neuroendocrine tumor and to correlate it with WHO classification of this tumor. METHODS： We retrospectively analyzed L1 expression in 63 cases of pancreatic neuroendocrine tumor by immunohistochemistry on paraffin sections of primary tumors or metastases. Staining was performed by peroxidase technique with monoclonal antibody U3127.11 against human L1. All tumors were classified according to WHO classification as well-differentiated neuroendo- crine tumors and carcinomas or poorly-differentiated neuroendocrine carcinomas. RESULTS： LI was detected in 5 （7.9%） of 63 pancreatic neuroendocrine tumors. Four （44.4%） of 9 poorlydifferentiated carcinomas expressed L1. In contrast, only 1 （1.9%） of 54 well-differentiated tumors or carcinomas was positive for LI. No expression was found in Langerhans islet cells of normal pancreatic tissue. Cross table analysis showed a significant association between L1 expression and classification of neuroendocrine tumors of the pancreas （P〈0.01）. CONCLUSION： L1 is specifically expressed in poorlydifferentiated pancreatic neuroendocrine carcinomas that are known to have the worst prognosis. L1 might be a marker for risk prediction of patients diagnosed with pancreatic neuroendocrine carcinomas.

关键词： Neuroendocrine pancreatic tumor Tumor markers Cell adhesion molecules L1

The interaction between KIF21A and KANK1 regulates dendritic morphology and synapse plasticity in neurons

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Neural Regeneration Research 2025年第1期20卷 209-223页

作者： Shi-Yan Sun Lingyun Nie Jing Zhang Xue Fang Hongmei Luo Chuanhai Fu Zhiyi Wei Ai-Hui Tang Hefei National Research center for Physical Sciences at the Microscale CAS Key Laboratory of Brain Function and DiseaseMinistry of Education Key Laboratory for Membrane-less Organelles and Cellular DynamicsDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina Institute of Artificial Intelligence Hefei Comprehensive National Science CenterHefeiAnhui ProvinceChina CAS center for Excellence in molecular Cell Sciences Division of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina Department of neurobiology School of Life SciencesSouthern University of Science and TechnologyShenzhenGuangdong ProvinceChina Brain Research center Southern University of Science and TechnologyShenzhenGuangdong ProvinceChina

Morphological alterations in dendritic spines have been linked to changes in functional communication between neurons that affect learning and ***-4 KIF21A helps organize the microtubule-actin network at the cell cortex by interacting with KANK1;however,whether KIF21A modulates dendritic structure and function in neurons remains *** this study,we found that KIF21A was distributed in a subset of dendritic spines,and that these KIF21A-positive spines were larger and more structurally plastic than KIF21A-negative ***,the interaction between KIF21A and KANK1 was found to be critical for dendritic spine morphogenesis and synaptic *** of either KIF21A or KANK1 inhibited dendritic spine morphogenesis and dendritic branching,and these deficits were fully rescued by coexpressing full-length KIF21A or KANK1,but not by proteins with mutations disrupting direct binding between KIF21A and KANK1 or binding between KANK1 and *** down KIF21A in the hippocampus of rats inhibited the amplitudes of long-term potentiation induced by high-frequency stimulation and negatively impacted the animals’cognitive *** together,our findings demonstrate the function of KIF21A in modulating spine morphology and provide insight into its role in synaptic function.

关键词： actin cytoskeleton dendrite KANK1 KIF21A microtubule spine morphology spine synaptic plasticity talin1