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Article ; Online: Neuronal vesicular trafficking and release in age-related cognitive impairment.

Deák, Ferenc

The journals of gerontology. Series A, Biological sciences and medical sciences

2014 Volume 69, Issue 11, Page(s) 1325–1330

Abstract: Aging is a common major risk factor for many neurological disorders resulting in cognitive impairment and neurodegeneration including Parkinson's and Alzheimer's diseases. Novel results from the fields of molecular neuroscience and aging research provide ...

Abstract	Aging is a common major risk factor for many neurological disorders resulting in cognitive impairment and neurodegeneration including Parkinson's and Alzheimer's diseases. Novel results from the fields of molecular neuroscience and aging research provide evidence for a link between decline of various cognitive, executive functions and changes in neuronal mechanisms of intracellular trafficking and regulated vesicle release processes in the aging nervous system. In this Perspective, we review these recent findings and formulate a hypothesis on how cargo delivery to the synapses and the release of neurotrophic factors may be involved in maintaining learning and memory capabilities during healthy aging and present examples on how defects of those disrupt normal cognition. We provide an overview of emerging new concepts and approaches that will significantly advance our understanding of the aging brain and pathophysiology of dementia. This knowledge will be instrumental in defining drug targets and designing novel therapeutic strategies.
MeSH term(s)	Actin Cytoskeleton/physiology ; Aging/physiology ; Aging/psychology ; Animals ; Brain/physiopathology ; CA1 Region, Hippocampal/physiopathology ; Cognition Disorders/physiopathology ; Humans ; Models, Neurological ; Molecular Motor Proteins/physiology ; Nerve Degeneration/physiopathology ; Nerve Growth Factors/physiology ; Neuronal Plasticity/physiology ; Neurons/physiology ; Receptors, AMPA/physiology ; Synaptic Transmission/physiology ; Synaptic Vesicles/physiology ; tau Proteins/physiology
Chemical Substances	Molecular Motor Proteins ; Nerve Growth Factors ; Receptors, AMPA ; tau Proteins
Language	English
Publishing date	2014-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glu061
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Article: Evaluation of Waldmann-type and Frenkel-type foot and mouth disease in pigs.

Solyom, F / Szent-Ivanyi, M / Deak, F

Revue scientifique et technique (International Office of Epizootics)

2017 Volume 3, Issue 2, Page(s) 351–367

Language	English
Publishing date	2017-12-13
Publishing country	France
Document type	Journal Article
ZDB-ID	792125-1
ISSN	1608-0637 ; 0253-1933
ISSN (online)	1608-0637
ISSN	0253-1933
DOI	10.20506/rst.3.2.161
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Article ; Online: Alterations in Alzheimer's disease microglia transcriptome might be involved in bone pathophysiology.

Gharpure, Mohini / Vyavahare, Sagar / Ahluwalia, Pankaj / Gupta, Sonu Kumar / Lee, Tae Jin / Lohakare, Jayant / Kolhe, Ravindra / Lei, Yun / Deak, Ferenc / Lu, Xin-Yun / Isales, Carlos M / Fulzele, Sadanand

Neurobiology of disease

2024 Volume 191, Page(s) 106404

Abstract: Aging is a major risk factor for multiple chronic disorders in the elderly population, including Alzheimer's disease (AD) and Osteoporosis. AD is a progressive neurodegenerative disease characterized by memory loss. In addition to dementia, several ... ...

Abstract	Aging is a major risk factor for multiple chronic disorders in the elderly population, including Alzheimer's disease (AD) and Osteoporosis. AD is a progressive neurodegenerative disease characterized by memory loss. In addition to dementia, several studies have shown that AD patients experience an increased rate of musculoskeletal co-morbidities, such as osteoporosis. Since tissue-specific macrophages contribute to both diseases, this study analyzed the microglia transcriptome of AD mice to determine a common gene signature involved in osteoclast biology. After comparing differentially regulated genes from GEO data sets (GSE93824 and GSE212277), there were 35 common upregulated genes and 89 common downregulated genes. Of these common genes, seven genes are known to play an important role in bone homeostasis. CSF1, SPP1, FAM20C, and Cst7 were upregulated and are associated with osteoclastogenesis and inflammation. Among the downregulated genes, LILRA6, MMP9, and COL18A1 are involved in bone formation and osteoclast regulation. We further validated some of these genes (CSF1, Cst7, and SPP1) in the cortex and the bone of AD mice models. The dysregulation of these microglial genes in AD might provide insights into the co-occurrence of AD and osteoporosis and offer potential therapeutic targets to combat disease progression.
MeSH term(s)	Aged ; Humans ; Mice ; Animals ; Alzheimer Disease/genetics ; Transcriptome ; Microglia ; Neurodegenerative Diseases ; Osteoporosis/genetics ; Calcium-Binding Proteins/genetics ; Extracellular Matrix Proteins
Chemical Substances	FAM20C protein, mouse ; Calcium-Binding Proteins ; Extracellular Matrix Proteins
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2024.106404
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Article ; Online: Age-Related Cognitive Impairment: Role of Reduced Synaptobrevin-2 Levels in Deficits of Memory and Synaptic Plasticity.

Orock, Albert / Logan, Sreemathi / Deak, Ferenc

The journals of gerontology. Series A, Biological sciences and medical sciences

2019 Volume 75, Issue 9, Page(s) 1624–1632

Abstract: Cognitive impairment in the aging population is quickly becoming a health care priority, for which currently no disease-modifying treatment is available. Multiple domains of cognition decline with age even in the absence of neurodegenerative diseases. ... ...

Abstract	Cognitive impairment in the aging population is quickly becoming a health care priority, for which currently no disease-modifying treatment is available. Multiple domains of cognition decline with age even in the absence of neurodegenerative diseases. The cellular and molecular changes leading to cognitive decline with age remain elusive. Synaptobrevin-2 (Syb2), the major vesicular SNAP receptor protein, highly expressed in the cerebral cortex and hippocampus, is essential for synaptic transmission. We have analyzed Syb2 protein levels in mice and found a decrease with age. To investigate the functional consequences of lower Syb2 expression, we have used adult Syb2 heterozygous mice (Syb2+/-) with reduced Syb2 levels. This allowed us to mimic the age-related decrease of Syb2 in the brain in order to selectively test its effects on learning and memory. Our results show that Syb2+/- animals have impaired learning and memory skills and they perform worse with age in the radial arm water maze assay. Syb2+/- hippocampal neurons have reduced synaptic plasticity with reduced release probability and impaired long-term potentiation in the CA1 region. Syb2+/- neurons also have lower vesicular release rates when compared to WT controls. These results indicate that reduced Syb2 expression with age is sufficient to cause cognitive impairment.
MeSH term(s)	Animals ; Blotting, Western ; Brain/metabolism ; Brain/physiopathology ; Cognitive Aging/physiology ; Heterozygote ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Maze Learning ; Memory Disorders/blood ; Memory Disorders/physiopathology ; Mice ; Mice, Knockout ; Neuronal Plasticity/physiology ; Vesicle-Associated Membrane Protein 2/analysis ; Vesicle-Associated Membrane Protein 2/metabolism
Chemical Substances	Vesicle-Associated Membrane Protein 2 ; vesicle-associated membrane protein 2, mouse
Language	English
Publishing date	2019-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glz013
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Article: Novel Cellular Functions of Very Long Chain-Fatty Acids: Insight From ELOVL4 Mutations.

Deák, Ferenc / Anderson, Robert E / Fessler, Jennifer L / Sherry, David M

Frontiers in cellular neuroscience

2019 Volume 13, Page(s) 428

Abstract: Elongation of Very Long chain fatty acids-4 (ELOVL4) protein is a member of the ELOVL family of fatty acid elongases that is collectively responsible for catalyzing formation of long chain fatty acids. ELOVL4 is the only family member that catalyzes ... ...

Abstract	Elongation of Very Long chain fatty acids-4 (ELOVL4) protein is a member of the ELOVL family of fatty acid elongases that is collectively responsible for catalyzing formation of long chain fatty acids. ELOVL4 is the only family member that catalyzes production of Very Long Chain Saturated Fatty Acids (VLC-SFA) and Very Long Chain Polyunsaturated Fatty Acids (VLC-PUFA) with chain lengths ≥28 carbons. ELOVL4 and its VLC-SFA and VLC-PUFA products are emerging as important regulators of synaptic signaling and neuronal survival in the central nervous system (CNS). Distinct sets of mutations in
Language	English
Publishing date	2019-09-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2019.00428
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Article ; Online: Munc18-1 haploinsufficiency impairs learning and memory by reduced synaptic vesicular release in a model of Ohtahara syndrome.

Orock, Albert / Logan, Sreemathi / Deak, Ferenc

Molecular and cellular neurosciences

2017 Volume 88, Page(s) 33–42

Abstract: Ohtahara syndrome, also known as type 4 of Early Infantile Epileptic Encephalopathy with suppression bursts (EIEE-4) is currently an untreatable disorder that presents with seizures and impaired cognition. EIEE-4 patients have mutations most frequently ... ...

Abstract	Ohtahara syndrome, also known as type 4 of Early Infantile Epileptic Encephalopathy with suppression bursts (EIEE-4) is currently an untreatable disorder that presents with seizures and impaired cognition. EIEE-4 patients have mutations most frequently in the STXBP1 gene encoding a Sec protein, munc18-1. The exact molecular mechanism of how these munc18-1 mutations cause impaired cognition, remains elusive. The leading haploinsufficiency hypothesis posits that mutations in munc18-1 render the protein unstable leading to its degradation. Expression driven by the healthy allele is not sufficient to maintain the physiological function resulting in haploinsufficiency. The aim of this study has been to understand how munc18-1 haploinsufficiency causes cognitive impairment seen in EIEE-4. Here we present results from behavioral to cellular effects from a mouse model of munc18-1 haploinsufficiency. Munc18-1 heterozygous knock-out mice showed impaired spatial learning and memory in behavior tests as well as reduced synaptic plasticity in hippocampal CA1 long-term potentiation. Cultured munc18-1 heterozygous hippocampal neurons had significantly slower rate of synaptic vesicle release and decreased readily releasable vesicle pool compared to wild-type control neurons in fluorescent FM dye assays. These results demonstrate that reduced munc18-1 levels are sufficient to impair learning and memory by reducing neurotransmitter release. Therefore, our study implicates munc18-1 haploinsufficiency as a primary cause of cognitive impairment seen in EIEE-4 patients.
MeSH term(s)	Animals ; Brain/physiopathology ; Haploinsufficiency/genetics ; Heterozygote ; Learning/physiology ; Memory/physiology ; Mice, Knockout ; Munc18 Proteins/genetics ; Mutation/genetics ; Neurons/metabolism ; Spasms, Infantile/genetics ; Synaptic Transmission/genetics ; Synaptic Vesicles/metabolism
Chemical Substances	Munc18 Proteins ; Stxbp1 protein, mouse
Language	English
Publishing date	2017-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2017.12.002
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Article ; Online: CRISPR-Cas9 Long-Read Sequencing for Mapping Transgenes in the Mouse Genome.

Bryant, W Bart / Yang, Allison / Griffin, Susan H / Zhang, Wei / Rafiq, Ashiq M / Han, Weiping / Deak, Ferenc / Mills, Mary Katherine / Long, Xiaochun / Miano, Joseph M

The CRISPR journal

2023 Volume 6, Issue 2, Page(s) 163–175

Abstract: Microinjected transgenes, both large and small, are known to insert randomly into the mouse genome. Traditional methods of mapping a transgene are challenging, thus complicating breeding strategies and accurate interpretation of phenotypes, particularly ... ...

Abstract	Microinjected transgenes, both large and small, are known to insert randomly into the mouse genome. Traditional methods of mapping a transgene are challenging, thus complicating breeding strategies and accurate interpretation of phenotypes, particularly when a transgene disrupts critical coding or noncoding sequences. As the vast majority of transgenic mouse lines remain unmapped, we developed CRISPR-Cas9 Long-Read Sequencing (CRISPR-LRS) to ascertain transgene integration loci. This novel approach mapped a wide size range of transgenes and uncovered more complex transgene-induced host genome re-arrangements than previously appreciated. CRISPR-LRS offers a facile, informative approach to establish robust breeding practices and will enable researchers to study a gene without confounding genetic issues. Finally, CRISPR-LRS will find utility in rapidly and accurately interrogating gene/genome editing fidelity in experimental and clinical settings.
MeSH term(s)	Animals ; Mice ; Gene Editing ; CRISPR-Cas Systems/genetics ; Transgenes ; Genome/genetics ; Mice, Transgenic
Language	English
Publishing date	2023-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3017891-5
ISSN	2573-1602 ; 2573-1599
ISSN (online)	2573-1602
ISSN	2573-1599
DOI	10.1089/crispr.2022.0099
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Zs.MG 119: Show issues

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Article ; Online: Aging, synaptic dysfunction, and insulin-like growth factor (IGF)-1.

Deak, Ferenc / Sonntag, William E

The journals of gerontology. Series A, Biological sciences and medical sciences

2012 Volume 67, Issue 6, Page(s) 611–625

Abstract: Insulin-like growth factor (IGF)-1 is an important neurotrophic hormone. Deficiency of this hormone has been reported to influence the genesis of cognitive impairment and dementia in the elderly patients. Nevertheless, there are studies indicating that ... ...

Abstract	Insulin-like growth factor (IGF)-1 is an important neurotrophic hormone. Deficiency of this hormone has been reported to influence the genesis of cognitive impairment and dementia in the elderly patients. Nevertheless, there are studies indicating that cognitive function can be maintained into old age even in the absence of circulating IGF-1 and studies that link IGF-1 to an acceleration of neurological diseases. Although IGF-1 has a complex role in brain function, synaptic effects appear to be central to the IGF-1-induced improvement in learning and memory. In this review, synaptic mechanisms of learning and memory and the effects of IGF-1 on synaptic communication are discussed. The emerging data indicate that synaptic function decreases with age and that IGF-1 contributes to information processing in the brain. Further studies that detail the specific actions of this important neurotrophic hormone will likely lead to therapies that result in improved cognitive function for the elderly patients.
MeSH term(s)	Aging/metabolism ; Aging/physiology ; Animals ; Cognition Disorders/metabolism ; Cognition Disorders/physiopathology ; Female ; Humans ; Insulin-Like Growth Factor I/metabolism ; Learning/physiology ; Long-Term Potentiation/physiology ; Male ; Mice ; Rats ; Synapses/metabolism ; Synapses/physiology
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2012-04-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/gls118
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Article: Matrilin-2, an extracellular adaptor protein, is needed for the regeneration of muscle, nerve and other tissues.

Korpos, Éva / Deák, Ferenc / Kiss, Ibolya

Neural regeneration research

2015 Volume 10, Issue 6, Page(s) 866–869

Abstract: The extracellular matrix (ECM) performs essential functions in the differentiation, maintenance and remodeling of tissues during development and regeneration, and it undergoes dynamic changes during remodeling concomitant to alterations in the cell-ECM ... ...

Abstract	The extracellular matrix (ECM) performs essential functions in the differentiation, maintenance and remodeling of tissues during development and regeneration, and it undergoes dynamic changes during remodeling concomitant to alterations in the cell-ECM interactions. Here we discuss recent data addressing the critical role of the widely expressed ECM protein, matrilin-2 (Matn2) in the timely onset of differentiation and regeneration processes in myogenic, neural and other tissues and in tumorigenesis. As a multiadhesion adaptor protein, it interacts with other ECM proteins and integrins. Matn2 promotes neurite outgrowth, Schwann cell migration, neuromuscular junction formation, skeletal muscle and liver regeneration and skin wound healing. Matn2 deposition by myoblasts is crucial for the timely induction of the global switch toward terminal myogenic differentiation during muscle regeneration by affecting transforming growth factor beta/bone morphogenetic protein 7/Smad and other signal transduction pathways. Depending on the type of tissue and the pathomechanism, Matn2 can also promote or suppress tumor growth.
Language	English
Publishing date	2015-06-25
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.158332
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Article ; Online: W246G Mutant ELOVL4 Impairs Synaptic Plasticity in Parallel and Climbing Fibers and Causes Motor Defects in a Rat Model of SCA34.

Nagaraja, Raghavendra Y / Sherry, David M / Fessler, Jennifer L / Stiles, Megan A / Li, Feng / Multani, Karanpreet / Orock, Albert / Ahmad, Mohiuddin / Brush, Richard S / Anderson, Robert E / Agbaga, Martin-Paul / Deák, Ferenc

Molecular neurobiology

2021 Volume 58, Issue 10, Page(s) 4921–4943

Abstract: Spinocerebellar ataxia (SCA) is a neurodegenerative disorder characterized by ataxia and cerebellar atrophy. A number of different mutations gives rise to different types of SCA with characteristic ages of onset, symptomatology, and rates of progression. ...

Abstract	Spinocerebellar ataxia (SCA) is a neurodegenerative disorder characterized by ataxia and cerebellar atrophy. A number of different mutations gives rise to different types of SCA with characteristic ages of onset, symptomatology, and rates of progression. SCA type 34 (SCA34) is caused by mutations in ELOVL4 (ELOngation of Very Long-chain fatty acids 4), a fatty acid elongase essential for biosynthesis of Very Long Chain Saturated and Polyunsaturated Fatty Acids (VLC-SFA and VLC-PUFA, resp., ≥28 carbons), which have important functions in the brain, skin, retina, Meibomian glands, testes, and sperm. We generated a rat model of SCA34 by knock-in of the SCA34-causing 736T>G (p.W246G) ELOVL4 mutation. Rats carrying the mutation developed impaired motor deficits by 2 months of age. To understand the mechanism of these motor deficits, we performed electrophysiological studies using cerebellar slices from rats homozygous for W246G mutant ELOVL4 and found marked reduction of long-term potentiation at parallel fiber synapses and long-term depression at climbing fiber synapses onto Purkinje cells. Neuroanatomical analysis of the cerebellum showed normal cytoarchitectural organization with no evidence of degeneration out to 6 months of age. These results point to ELOVL4 as essential for motor function and cerebellar synaptic plasticity. The results further suggest that ataxia in SCA34 patients may arise from a primary impairment of synaptic plasticity and cerebellar network desynchronization before onset of neurodegeneration and progression of the disease at a later age.
MeSH term(s)	Animals ; Cerebellum/pathology ; Eye Proteins/genetics ; Female ; Male ; Membrane Proteins/genetics ; Motor Disorders/genetics ; Motor Disorders/pathology ; Mutation/genetics ; Nerve Fibers, Myelinated/pathology ; Neuronal Plasticity/physiology ; Organ Culture Techniques ; Rats ; Rats, Long-Evans ; Rats, Transgenic ; Spinocerebellar Ataxias/genetics ; Spinocerebellar Ataxias/pathology
Chemical Substances	Elovl4 protein, mouse ; Eye Proteins ; Membrane Proteins
Language	English
Publishing date	2021-07-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-021-02439-1
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