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DTSTART;TZID=Europe/Madrid:20250901T100000
DTEND;TZID=Europe/Madrid:20250901T190000
DTSTAMP:20260525T135656
CREATED:20250328T102240Z
LAST-MODIFIED:20250905T081426Z
UID:64599-1756720800-1756753200@bio-gipuzkoa.eus
SUMMARY:Neuromuscular junction in amyotrophic lateral sclerosis: Study of the pathological mechanisms
DESCRIPTION:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\, it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death. \n\nWhich postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death.\nHypothesis has been addressed by focusing on the contribution of different cell types\, thus allowing a more comprehensive view of the NMJ environment.\nFinally\, it has been shown that muscle signalling is also altered in ALS\, which could negatively affect NMJ formation and\, consequently.\nContribute to the pathogenesis of the disease. These findings place the skeletal muscle as a possible target for future therapeutic strategies\, opening new possibilities for the treatment of the disease through therapeutic approaches aimi.\n\nIn this PhD Thesis we have studied the pathological events underlying the neuromuscular junction dismantlement in the early stages of ALS disease\, which may provoke a retrograde stress resulting in the dismantling of the NMJ and the subsequent dying-back phenomenon. This hypothesis has been addressed by focusing on the contribution of different cell types\, thus allowing a more comprehensive view of the NMJ environment. Finally\, it has been shown that muscle signalling is also altered in ALS\,. \n\nWhich postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death.\nHypothesis has been addressed by focusing on the contribution of different cell types\, thus allowing a more comprehensive view of the NMJ environment.\nFinally\, it has been shown that muscle signalling is also altered in ALS\, which could negatively affect NMJ formation and\, consequently.\nContribute to the pathogenesis of the disease. These findings place the skeletal muscle as a possible target for future therapeutic strategies\, opening new possibilities for the treatment of the disease through therapeutic approaches aimi.\n\nhich could negatively affect NMJ formation and\, consequently\, contribute to the pathogenesis of the disease. These findings place the skeletal muscle as a possible target for future therapeutic strategies\, opening new possibilities for the treatment of the disease through therapeutic approaches aiming to restore or modulate its function at the NMJ level. \n \nAmyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\, it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\,it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death.
URL:https://bio-gipuzkoa.eus/agenda/neuromuscular-junction-in-amyotrophic-lateral-sclerosis-study-of-the-pathological-mechanisms/
LOCATION:Biogipuzkoa\, Pº Dr. Beguiristain s/n\, Donostia\, Gipuzkoa\, 20014\, Spain
CATEGORIES:Agenda
ATTACH;FMTTYPE=image/jpeg:https://bio-gipuzkoa.eus/wp-content/uploads/2025/02/31755dfa71b2e6cf0156c91bf5131863-1.jpeg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20250926T100000
DTEND;TZID=Europe/Madrid:20250926T100000
DTSTAMP:20260525T135656
CREATED:20250620T104235Z
LAST-MODIFIED:20250905T081321Z
UID:77140-1758880800-1758880800@bio-gipuzkoa.eus
SUMMARY:Neurodegenerative disease characterised by the death
DESCRIPTION:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\, it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death. \nIn this PhD Thesis we have studied the pathological events underlying the neuromuscular junction dismantlement in the early stages of ALS disease\, which may provoke a retrograde stress resulting in the dismantling of the NMJ and the subsequent dying-back phenomenon. This hypothesis has been addressed by focusing on the contribution of different cell types\, thus allowing a more comprehensive view of the NMJ environment. Finally\, it has been shown that muscle signalling is also altered in ALS\, which could negatively affect NMJ formation and\, consequently\, contribute to the pathogenesis of the disease. These findings place the skeletal muscle as a possible target for future therapeutic strategies\, opening new possibilities for the treatment of the disease through therapeutic approaches aiming to restore or modulate its function at the NMJ level.
URL:https://bio-gipuzkoa.eus/agenda/mechanisms-and-altered-signalling-in-its-microenvironment-2/
LOCATION:Biogipuzkoa\, Pº Dr. Beguiristain s/n\, Donostia\, Gipuzkoa\, 20014\, Spain
CATEGORIES:Seminarios
ATTACH;FMTTYPE=image/jpeg:https://bio-gipuzkoa.eus/wp-content/uploads/2024/07/n3.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20250927T120000
DTEND;TZID=Europe/Madrid:20250927T140000
DTSTAMP:20260525T135656
CREATED:20250620T104604Z
LAST-MODIFIED:20250905T081347Z
UID:77144-1758974400-1758981600@bio-gipuzkoa.eus
SUMMARY:Neuromuscular junction in amyotrophic lateral sclerosis: Study of the pathological mechanisms
DESCRIPTION:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\, it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death.
URL:https://bio-gipuzkoa.eus/agenda/neuromuscular-junction-in-amyotrophic-lateral-sclerosis-study-of-the-pathological-mechanisms-2/
LOCATION:Biogipuzkoa\, Pº Dr. Beguiristain s/n\, Donostia\, Gipuzkoa\, 20014\, Spain
CATEGORIES:Tesis Doctorales
ATTACH;FMTTYPE=image/jpeg:https://bio-gipuzkoa.eus/wp-content/uploads/2025/02/31755dfa71b2e6cf0156c91bf5131863-1.jpeg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20250929T100000
DTEND;TZID=Europe/Madrid:20250929T150000
DTSTAMP:20260525T135656
CREATED:20250319T140130Z
LAST-MODIFIED:20250905T081300Z
UID:5195-1759140000-1759158000@bio-gipuzkoa.eus
SUMMARY:Study of the pathological mechanisms and altered signalling in its microenvironment
DESCRIPTION:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\, it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death. \nIn this PhD Thesis we have studied the pathological events underlying the neuromuscular junction dismantlement in the early stages of ALS disease\, which may provoke a retrograde stress resulting in the dismantling of the NMJ and the subsequent dying-back phenomenon. This hypothesis has been addressed by focusing on the contribution of different cell types\, thus allowing a more comprehensive view of the NMJ environment. Finally\, it has been shown that muscle signalling is also altered in ALS\, which could negatively affect NMJ formation and\, consequently\, contribute to the pathogenesis of the disease. These findings place the skeletal muscle as a possible target for future therapeutic strategies\, opening new possibilities for the treatment of the disease through therapeutic approaches aiming to restore or modulate its function at the NMJ level.
URL:https://bio-gipuzkoa.eus/agenda/evento-de-prueba-1/
LOCATION:Biogipuzkoa\, Pº Dr. Beguiristain s/n\, Donostia\, Gipuzkoa\, 20014\, Spain
CATEGORIES:Agenda
ATTACH;FMTTYPE=image/jpeg:https://bio-gipuzkoa.eus/wp-content/uploads/2025/03/img_recurso_9l6a9033.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20250930T100000
DTEND;TZID=Europe/Madrid:20250930T170000
DTSTAMP:20260525T135656
CREATED:20250328T102206Z
LAST-MODIFIED:20250905T081222Z
UID:64595-1759226400-1759251600@bio-gipuzkoa.eus
SUMMARY:Mechanisms and altered signalling in its microenvironment
DESCRIPTION:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by the death of upper and lower motor neurons (MN) and severe muscle atrophy. In recent years\, it has been shown that the degeneration MNs can also be caused or exacerbated by other neighbouring cells such as glial cells or skeletal muscle\, and these are also known as non-cell autonomous mechanisms. Regarding skeletal muscle\, muscle atrophy is not a mere result of denervation\, but ALS patients and animal models show intrinsic muscle defects independently of MN degeneration. Likewise\, synapses between motor nerve terminals and skeletal muscle fibres occur at the neuromuscular junction (NMJ). Defects in NMJs prior to MN degeneration or symptom onset have also been widely reported in ALS\, leading to the proposal of the ‘dying-back’ theory\, which postulates that MN defects begin at the distal nerve terminals located in the NMJ\, and are transmitted retrogradely to the MN soma\, ultimately inducing its death. \nIn this PhD Thesis we have studied the pathological events underlying the neuromuscular junction dismantlement in the early stages of ALS disease\, which may provoke a retrograde stress resulting in the dismantling of the NMJ and the subsequent dying-back phenomenon. This hypothesis has been addressed by focusing on the contribution of different cell types\, thus allowing a more comprehensive view of the NMJ environment. Finally\, it has been shown that muscle signalling is also altered in ALS\, which could negatively affect NMJ formation and\, consequently\, contribute to the pathogenesis of the disease. These findings place the skeletal muscle as a possible target for future therapeutic strategies\, opening new possibilities for the treatment of the disease through therapeutic approaches aiming to restore or modulate its function at the NMJ level.
URL:https://bio-gipuzkoa.eus/agenda/mechanisms-and-altered-signalling-in-its-microenvironment/
LOCATION:Biogipuzkoa\, Pº Dr. Beguiristain s/n\, Donostia\, Gipuzkoa\, 20014\, Spain
CATEGORIES:Congresos/ Jornadas/ Otros
ATTACH;FMTTYPE=image/jpeg:https://bio-gipuzkoa.eus/wp-content/uploads/2025/03/vincenzo-roca.jpg
END:VEVENT
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