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Tart cherry extract and omega fatty acids reduce behavioral deficits, gliosis, and amyloid-beta deposition in the 5xFAD mouse model of Alzheimer’s disease
Bowers Z, Maiti P, Bourcier A, Morse J, Jenrow K, Rossignol J, Dunbar GL (2021) Tart cherry extract and omega fatty acids reduce behavioral deficits, gliosis, and amyloid-beta deposition in the 5xFAD mouse model of Alzheimer’s disease. Brain Sci 11(11):1423. doi: 10.3390/brainsci11111423 PMID: 34827424
Objective: To assess the efficacy of Total Body Rhythm (TBR) for treating behavioral and neuropathological deficits in the 5xFAD model of AD.
Summary: The combination of tart cherry extract and omega fatty acids in TBR can reduce AD-like deficits in 5xFAD mice.
Usage: Previous work demonstrated that TBR can prevent loss of body weight in a mu p75-SAP mouse model of AD.
Related Products: mu p75-SAP (Cat. #IT-16)
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Engrafted stem cell therapy for Alzheimer’s disease: A promising treatment strategy with clinical outcome
Salwa, LK (2021) Engrafted stem cell therapy for Alzheimer’s disease: A promising treatment strategy with clinical outcome. J Control Release 338:837-857. doi: 10.1016/j.jconrel.2021.09.007
Objective: This review provides a detailed update on stem cell therapy (SCT) for Alzheimer’s Disease (AD)
Summary: What future holds for SCT in the treatment of AD is summarized
Usage: Liu et al. injected 1.5 μg of mu p75-SAP into the medial septum.
Read the featured article in Targeting Trends.
Related Products: mu p75-SAP (Cat. #IT-16)
Overexpression of nerve growth factor in the hippocampus induces behavioral changes in rats with 192IgG-saporin-induced cholinergic deficit
Dobryakova YV, Zaichenko MI, Spivak YS, Stepanichev MY, Markevich VA, Bolshakov AP (2021) Overexpression of nerve growth factor in the hippocampus induces behavioral changes in rats with 192IgG-saporin-induced cholinergic deficit. Neurochem J 15:273-281. doi: 10.1134/S1819712421030028
Summary: Degeneration of septal cholinergic neurons caused by the immunotoxin 192-IgG-SAP produces a model of the pathological state that occurs in Alzheimer’s Disease. This study investigated whether overexpression of NGF in the hippocampus, where septal neurons send their projections, may reduce the consequences of this damage. Data suggest that NGF overexpression in the hippocampus of rats may partly compensate some 192 IgG-SAP-induced impairments related to cholinergic deficit.
Usage: 192-IgG-SAP or an equivalent volume of PBS (4 µg/site) was administered bilaterally into the ventricles.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Cholinergic modulation of sensory processing in awake mouse cortex
Jimenez-Martin J, Potapov D, Potapov K, Knöpfel T, Empson RM (2021) Cholinergic modulation of sensory processing in awake mouse cortex. Sci Rep 11(1):17525. doi: 10.1038/s41598-021-96696-8
Objective: To decipher the timing and significance of acetylcholine actions.
Summary: Study provides new insights into how the cortex processes sensory information and how loss of acetylcholine, for example in Alzheimer’s Disease, disrupts sensory behaviours.
Usage: Focal cortical injection of mu p75-SAP or Rabbit IgG-SAP (1.7 mg/ml, 0.3 µl total volume, rate 0.075 µl/minute).
Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)
Therapeutic agent delivery across the blood-brain barrier using focused ultrasound
McMahon D, O’Reilly MA, Hynynen K (2021) Therapeutic agent delivery across the blood-brain barrier using focused ultrasound. Annu Rev Biomed Eng 23:89-113. doi: 10.1146/annurev-bioeng-062117-121238 PMID: 33752471
Summary: Review of the use of focused ultrasound, in combination with circulating microbubbles, can be used to transiently and noninvasively increase cerebrovascular permeability with a high level of spatial precision. For minutes to hours following sonication, drugs can be administered systemically to extravasate in the targeted brain regions and exert a therapeutic effect, after which permeability returns to baseline levels.
Usage: Shin et al. reported improved spatial memory following FUS+MB exposure in a rat model of cholinergic neuron degeneration. 192-IgG-SAP was injected bilaterally into the lateral ventricle (4 μl at a concentration of 0.63 μg/μl at a rate of 1 μl/min).
Related Products: 192-IgG-SAP (Cat. #IT-01)
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Neurotoxic effects, mechanisms, and outcome of 192 IgG-Saporin lesions.
Petrosini L, De Bartolo P, Cutuli D (2021) Neurotoxic effects, mechanisms, and outcome of 192 IgG-Saporin lesions. RM Kostrzewa (Ed.): Handbook of Neurotoxicity . Springer, Cham doi: 10.1007/978-3-030-71519-9_79-1
Summary: 192-IgG-saporin selectively destroys basal forebrain cholinergic neurons that provide cholinergic input to the hippocampus, entire cortical mantle, amygdala, and olfactory bulb. Immunotoxic lesions by 192-IgG-saporin represent a valid animal model of Alzheimer’s disease, given the degeneration of basal cholinergic system present in this pathology. The selective lesioning of cholinergic innervation by means of 192-IgG-saporin (injected i.p. or i.c.v.) is able to interfere with experience-dependent plasticity.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Specific phospholipid modulation by muscarinic signaling in a rat lesion model of Alzheimer’s disease
Llorente-Ovejero A, Martínez-Gardeazabal J, Moreno-Rodríguez M, Lombardero L, González de San Román E, Manuel I, Giralt MT, Rodríguez-Puertas R (2021) Specific phospholipid modulation by muscarinic signaling in a rat lesion model of Alzheimer’s disease. ACS Chem Neurosci 12(12):2167-2181. doi: 10.1021/acschemneuro.1c00169 PMID: 34037379
Objective: To evaluate the lipid composition and muscarinic signaling in brain areas related to cognitive processes.
Summary: Using a rat model of BFCN lesion, this study evaluated the lipid composition and muscarinic signaling in brain areas related to cognitive processes. Results suggest that the modulation of specific lipid metabolic routes could represent an alternative therapeutic strategy to potentiate cholinergic neurotransmission and preserve cell membrane integrity in AD.
Usage: 192-IgG-SAP was dissolved in aCSF under aseptic conditions to a final concentration of 130 ng/ml. aCSF or 192-IgG-SAP was bilaterally injected (1 ml/hemisphere) at a constant rate of 0.2 ml/min. to selectively eliminate BFCN in the NBM.
Related Products: 192-IgG-SAP (Cat. #IT-01)
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Tart cherry (fruit of prunus cerasus) concentrated powder (tccp) ameliorates glucocorticoid-induced muscular atrophy in mice.
Ku SK, Lim JM, Cho HR, Bashir KMI, Kim YS, Choi JS (2021) Tart cherry (fruit of prunus cerasus) concentrated powder (tccp) ameliorates glucocorticoid-induced muscular atrophy in mice. Medicina (Kaunas) 57(5):485. doi: 10.3390/medicina57050485 PMID: 34066110
Summary: Tart cherries have shown memory impairment lowering properties.
Related Products: mu p75-SAP (Cat. #IT-16)
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Reversal of object recognition memory deficit in perirhinal cortex-lesioned rats and primates and in rodent models of aging and alzheimer’s diseases.
Masmudi-Martín M, Navarro-Lobato I, López-Aranda MF, Browning PGF, Simón A-M, López-Téllez JF, Jiménez-Recuerda I, Martîn-Montañez E, Pérez-Mediavilla A, Frechilla D, Baxter MG, Khan ZU (2020) Reversal of object recognition memory deficit in perirhinal cortex-lesioned rats and primates and in rodent models of aging and alzheimer’s diseases. Neuroscience 448:287-298. doi: 10.1016/j.neuroscience.2020.08.039
Objective: To determine if Object Recognition Memory (ORM) can be restored.
Summary: Memory-deficient rats were generated by induction of lesions to the perirhinal cortex (PRh) through an injection of OX7-SAP. Expression of regulator of G-protein signaling 14 of 414 amino acids (RGS14414) restored ORM in memory-deficient PRh-lesioned rats and nonhuman primates. This treatment was sufficient for full recovery of ORM in rodent models of aging and Alzheimer’s disease.
Usage: Rats were injected with OX7-SAP (0.9 mg in 1ml) in the PRh of the brain.
Related Products: OX7-SAP (Cat. #IT-02)
Evaluation of the adverse effects of chronic exposure to donepezil (an acetylcholinesterase inhibitor) in adult zebrafish by behavioral and biochemical assessments.
Audira G, Ngoc Anh NT, Ngoc Hieu BT, Malhotra N, Siregar P, Villalobos O, Villaflores OB, Ger TR, Huang JC, Chen KH, Hsiao CD (2020) Evaluation of the adverse effects of chronic exposure to donepezil (an acetylcholinesterase inhibitor) in adult zebrafish by behavioral and biochemical assessments. Biomolecules 10(9):1340. doi: 10.3390/biom10091340 PMID: 32962160
Objective: The authors use zebrafish to conduct a deeper analysis of the potential adverse effects of DPZ on the short-term memory and behaviors of normal zebrafish by performing multiple behavioral and biochemical assays.
Summary: Chronic waterborne exposure to donepezil (DPZ) can severely induce adverse effects on normal zebrafish in a dose-dependent manner.
Related Products: 192-IgG-SAP (Cat. #IT-01)
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