Non-invasive Brain Delivery and Efficacy of BDNF in APP/PS1 Transgenic Mice

Kopec, Brian M.; Zhao, Lijun; Rosa‐Molinar, Eduardo; Siahaan, Teruna J.

doi:10.18103/mra.v8i2.2043

Cited by 17 publications

(13 citation statements)

References 65 publications

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“…An in vitro study shows that Aβ plays a role in reducing BDNF level (Zheng et al, 2010), which may lead to impaired synaptic plasticity. Intravenous infusion of BDNF with ADTC5, a blood brain barrier modulator, increased the level of BDNF in the hippocampus of APP/PS1 mice and increased BDNF was associated with higher efficacy in NOR and Y-maze tasks (Kopec et al, 2020). Neonatal TS from day 8-14 has proven to be beneficial in increasing BDNF level, and TS from day 1-7 and day 15-21 hasve been shown to reduce glucocorticoid receptors in the hippocampus in adult rats (Antoniazzi et al, 2016).…”

Section: Early Ts Reduces the Aβ Pathology In Adult Offspring At 2 An...mentioning

confidence: 99%

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APP^NL-G-FAdult Offspring^{NL-G-F/NL-G-F}mice

Hossain

Jafari

Karem

et al. 2022

Preprint

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Alzheimer Disease (AD) is associated with cerebral plaques and tangles, reduced synapse number, and shrinkage in several brain areas and these morphological effects are associated with the onset of compromised cognitive, motor, and anxiety-like behaviours. The focus of this study was to examine the effect of neonatal tactile stimulation on AD-like behavioural and neurological symptoms on APP NL-G-F/NL-G-F mice, a mouse model of AD. Our findings indicate that neonatal tactile stimulation improves cognition, motor skills, and anxiety-like symptoms in both offspring of stressed (dams exposed to gestational noise stress) and non-stressed APP mice and that these alterations are associated with reduced Aβ plaque formation. Thus, tactile stimulation appears to be a promising non-invasive preventative strategy for slowing the onset of dementia in aging animals.

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Section: Early Ts Reduces the Aβ Pathology In Adult Offspring At 2 An...mentioning

confidence: 99%

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APP^NL-G-FAdult Offspring^{NL-G-F/NL-G-F}mice

Hossain

Jafari

Karem

et al. 2022

Preprint

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“…However, there might be an alternative pathway to ensure sufficient remyelination or decrease axonal loss without upregulation of ERK. Increased expression of BDNF and its corresponding receptor TrkB could possibly enhance remyelination [61].…”

Section: Discussionmentioning

confidence: 99%

Oligodendrocyte-Specific Deletion of FGFR1 Reduces Cerebellar Inflammation and Neurodegeneration in MOG35-55-Induced EAE

Rajendran

Giraldo-Velásquez

et al. 2021

IJMS

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Multiple sclerosis (MS) is a chronic inflammatory and degenerative disease of the central nervous system (CNS). MS commonly affects the cerebellum causing acute and chronic symptoms. Cerebellar signs significantly contribute to clinical disability, and symptoms such as tremor, ataxia, and dysarthria are difficult to treat. Fibroblast growth factors (FGFs) and their receptors (FGFRs) are involved in demyelinating pathologies such as MS. In autopsy tissue from patients with MS, increased expression of FGF1, FGF2, FGF9, and FGFR1 was found in lesion areas. Recent research using mouse models has focused on regions such as the spinal cord, and data on the expression of FGF/FGFR in the cerebellum are not available. In recent EAE studies, we detected that oligodendrocyte-specific deletion of FGFRs results in a milder disease course, less cellular infiltrates, and reduced neurodegeneration in the spinal cord. The objective of this study was to characterize the role of FGFR1 in oligodendrocytes in the cerebellum. Conditional deletion of FGFR1 in oligodendrocytes (Fgfr1ind−/−) was achieved by tamoxifen application, EAE was induced using the MOG35-55 peptide. The cerebellum was analyzed by histology, immunohistochemistry, and western blot. At day 62 p.i., Fgfr1ind−/− mice showed less myelin and axonal degeneration compared to FGFR1-competent mice. Infiltration of CD3(+) T cells, Mac3(+) cells, B220(+) B cells and IgG(+) plasma cells in cerebellar white matter lesions (WML) was less in Fgfr1ind−/−mice. There were no effects on the number of OPC or mature oligodendrocytes in white matter lesion (WML). Expression of FGF2 and FGF9 associated with less myelin and axonal degeneration, and of the pro-inflammatory cytokines IL-1β, IL-6, and CD200 was downregulated in Fgfr1ind−/−mice. The FGF/FGFR signaling protein pAkt, BDNF, and TrkB were increased in Fgfr1ind−/−mice. These data suggest that cell-specific deletion of FGFR1 in oligodendrocytes has anti-inflammatory and neuroprotective effects in the cerebellum in the EAE disease model of MS.

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“…Therefore, some BBB modulators, such as cadherin peptides (ADTC5), have been used to improve BDNF’s efficiency in crossing the BBB. Intravenous injection of BDNF with ADTC5 in transgenic APP.PS1 mice improved the cognitive performance of these AD mice compared to BDNF alone [ 103 ].…”

Section: Growth Factors In Brain Function and Admentioning

confidence: 99%

Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

Gascon

Jann

Langlois-Blais

et al. 2021

IJMS

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Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations.

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Non-invasive Brain Delivery and Efficacy of BDNF in APP/PS1 Transgenic Mice

Cited by 17 publications

References 65 publications

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APP^NL-G-FAdult Offspring^{NL-G-F/NL-G-F}mice

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APP^NL-G-FAdult Offspring^{NL-G-F/NL-G-F}mice

Oligodendrocyte-Specific Deletion of FGFR1 Reduces Cerebellar Inflammation and Neurodegeneration in MOG35-55-Induced EAE

Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

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Non-invasive Brain Delivery and Efficacy of BDNF in APP/PS1 Transgenic Mice

Cited by 17 publications

References 65 publications

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APPNL-G-FAdult OffspringNL-G-F/NL-G-Fmice

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APPNL-G-FAdult OffspringNL-G-F/NL-G-Fmice

Oligodendrocyte-Specific Deletion of FGFR1 Reduces Cerebellar Inflammation and Neurodegeneration in MOG35-55-Induced EAE

Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

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Product

Resources

About

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APP^NL-G-FAdult Offspring^{NL-G-F/NL-G-F}mice

Early Tactile Stimulation Influences the Development of Alzheimer Disease in Gestationally Stressed APP^NL-G-FAdult Offspring^{NL-G-F/NL-G-F}mice