Abstract
| Original language | English |
|---|---|
| Article number | 304 |
| Journal | Front. Neurosci. |
| Volume | 13 |
| DOIs | |
| Publication status | Published - 2019 |
Keywords
- Autoimmunity
- Frontotemporal dementia
- Frontotemporal lobar degeneration
- Glutamate
- Neurotransmitter
- Transcranial magnetic stimulation
- 4 aminobutyric acid
- AMPA receptor
- dopamine
- glutamic acid
- neurotransmitter
- placebo
- serotonin
- serotonin uptake inhibitor
- disease exacerbation
- frontal cortex
- frontotemporal dementia
- glutamatergic synapse
- human
- molecular biology
- neurophysiology
- neurotransmission
- nonhuman
- Parkinson disease
- pathogenesis
- pyramidal nerve cell
- Review
- temporal cortex
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Toward a glutamate hypothesis of frontotemporal dementia : Frontiers in Neuroscience. / Benussi, A.; Alberici, A.; Buratti, E.; Ghidoni, R.; Gardoni, F.; Luca, M.D.; Padovani, A.; Borroni, B.
In: Front. Neurosci., Vol. 13, 304, 2019.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Toward a glutamate hypothesis of frontotemporal dementia
T2 - Frontiers in Neuroscience
AU - Benussi, A.
AU - Alberici, A.
AU - Buratti, E.
AU - Ghidoni, R.
AU - Gardoni, F.
AU - Luca, M.D.
AU - Padovani, A.
AU - Borroni, B.
N1 - Cited By :3 Export Date: 10 February 2020 Correspondence Address: Borroni, B.; Neurology Unit, Department of Clinical and Experimental Sciences, University of BresciaItaly; email: BarbaraBorronibarbara.borroni@unibs.it Chemicals/CAS: 4 aminobutyric acid, 28805-76-7, 56-12-2; dopamine, 51-61-6, 62-31-7; glutamic acid, 11070-68-1, 138-15-8, 56-86-0, 6899-05-4; serotonin, 50-67-9 Funding text 1: This work was supported by the Italian Ministry of Health (Ricerca Corrente). References: Adamczyk, A., Mejias, R., Takamiya, K., Yocum, J., Krasnova, I.N., Calderon, J., GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum (2012) Behav. Brain Res., 229, pp. 265-272; Alberici, A., Cristillo, V., Gazzina, S., Benussi, A., Padovani, A., Borroni, B., Autoimmunity and frontotemporal dementia (2018) Curr. 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PY - 2019
Y1 - 2019
N2 - Frontotemporal dementia (FTD) is a heterogenous neurodegenerative disorder, characterized by diverse clinical presentations, neuropathological characteristics and underlying genetic causes. Emerging evidence has shown that FTD is characterized by a series of changes in several neurotransmitter systems, including serotonin, dopamine, GABA and, above all, glutamate. Indeed, several studies have now provided preclinical and clinical evidence that glutamate is key in the pathogenesis of FTD. Animal models of FTD have shown a selective hypofunction in N-methyl D-aspartate (NMDA) and α-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, while in patients, glutamatergic pyramidal neurons are depleted in several areas, including the frontal and temporal cortices. Recently, a selective involvement of the AMPA GluA3 subunit has been observed in patients with autoimmune anti-GluA3 antibodies, which accounted for nearly 25% of FTD patients, leading to a decrease of the GluA3 subunit synaptic localization of the AMPA receptor and loss of dendritic spines. Other in vivo evidence of the involvement of the glutamatergic system in FTD derives from non-invasive brain stimulation studies using transcranial magnetic stimulation, in which specific stimulation protocols have indirectly identified a selective and prominent impairment in glutamatergic circuits in patients with both sporadic and genetic FTD. In view of limited disease modifying therapies to slow or revert disease progression in FTD, an important approach could consist in targeting the neurotransmitter deficits, similarly to what has been achieved in Parkinson's disease with dopaminergic therapy or Alzheimer's disease with cholinergic therapy. In this review, we summarize the current evidence concerning the involvement of the glutamatergic system in FTD, suggesting the development of new therapeutic strategies. © 2019 Benussi, Alberici, Buratti, Ghidoni, Gardoni, Di Luca, Padovani and Borroni.
AB - Frontotemporal dementia (FTD) is a heterogenous neurodegenerative disorder, characterized by diverse clinical presentations, neuropathological characteristics and underlying genetic causes. Emerging evidence has shown that FTD is characterized by a series of changes in several neurotransmitter systems, including serotonin, dopamine, GABA and, above all, glutamate. Indeed, several studies have now provided preclinical and clinical evidence that glutamate is key in the pathogenesis of FTD. Animal models of FTD have shown a selective hypofunction in N-methyl D-aspartate (NMDA) and α-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, while in patients, glutamatergic pyramidal neurons are depleted in several areas, including the frontal and temporal cortices. Recently, a selective involvement of the AMPA GluA3 subunit has been observed in patients with autoimmune anti-GluA3 antibodies, which accounted for nearly 25% of FTD patients, leading to a decrease of the GluA3 subunit synaptic localization of the AMPA receptor and loss of dendritic spines. Other in vivo evidence of the involvement of the glutamatergic system in FTD derives from non-invasive brain stimulation studies using transcranial magnetic stimulation, in which specific stimulation protocols have indirectly identified a selective and prominent impairment in glutamatergic circuits in patients with both sporadic and genetic FTD. In view of limited disease modifying therapies to slow or revert disease progression in FTD, an important approach could consist in targeting the neurotransmitter deficits, similarly to what has been achieved in Parkinson's disease with dopaminergic therapy or Alzheimer's disease with cholinergic therapy. In this review, we summarize the current evidence concerning the involvement of the glutamatergic system in FTD, suggesting the development of new therapeutic strategies. © 2019 Benussi, Alberici, Buratti, Ghidoni, Gardoni, Di Luca, Padovani and Borroni.
KW - Autoimmunity
KW - Frontotemporal dementia
KW - Frontotemporal lobar degeneration
KW - Glutamate
KW - Neurotransmitter
KW - Transcranial magnetic stimulation
KW - 4 aminobutyric acid
KW - AMPA receptor
KW - dopamine
KW - glutamic acid
KW - neurotransmitter
KW - placebo
KW - serotonin
KW - serotonin uptake inhibitor
KW - disease exacerbation
KW - frontal cortex
KW - frontotemporal dementia
KW - glutamatergic synapse
KW - human
KW - molecular biology
KW - neurophysiology
KW - neurotransmission
KW - nonhuman
KW - Parkinson disease
KW - pathogenesis
KW - pyramidal nerve cell
KW - Review
KW - temporal cortex
U2 - 10.3389/fnins.2019.00304
DO - 10.3389/fnins.2019.00304
M3 - Article
VL - 13
JO - Front. Neurosci.
JF - Front. Neurosci.
SN - 1662-4548
M1 - 304
ER -