Overview on Rodent Models of Alzheimer's Disease

Dodart, Jean-Cosme; May, Patrick C.

doi:10.1002/0471142301.ns0922s33

Cited by 25 publications

(23 citation statements)

References 138 publications

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“…The FTIR spectra gave information about the functional groups or chemical entities present in lupeol which was found in accordance with the literature data of lupeol [33]. Further 1H NMR spectrum of the compound revealed the presence of seven tertiary methyl protons, a sextet of one proton at δ 2.17 and presence of olefinic protons at (H-29a and b) which is characteristic of lupeol [34]. On the basis of FTIR and NMR spectra structure of compound was drawn which was in good conformity for the structure of lupeol (Figure 1).…”

Section: Isolation Of Lupeolsupporting

confidence: 85%

Lupeol Isolated from Betula alnoides Ameliorates Amyloid Beta Induced Neuronal Damage via Targeting Various Pathological Events and Alteration in Neurotransmitter Levels in Rat’s Brain

Kaundal¹,

Akhtar²,

Deshmukh³

2017

J Neurol Neurosci

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Lupeol, a natural active constituent of Betula alnoides (BA), is well known for its anti-inflammatory, anti-oxidant and neuroprotective activities. In present study the therapeutic potential of lupeol was investigated against amyloid beta (Aβ (1-42) ) induced cognitive deficit, neurochemical and biochemical abnormalities in rats. Lupeol was isolated from the BA and its structure was confirmed through nuclear magnetic resonance spectra. Aβ (1-42) (4 μg/4 μL) intracerebroventrically (icv) was administered to rats for the induction of Alzheimer's disease (AD). Lupeol treatment (25 mg/kg/day, 50 mg/kg/day and 100 mg/kg/day per orally) was started one week after Aβ (1-42) infusion up to the 21 st days. Morris water maze from day 16 to 21 and object recognition tasks on day 14 and 15 were performed for memory assessment. On 22 nd day, animals were sacrificed and hippocampi were isolated for analysis of biochemical (acetylcholinesterase, lipid hydroperoxide, glutathione and nitrite) and neuro-inflammatory (tumor necrosis factor -α, interleukin (IL)-1β, and IL-6) parameters. In the present study Aβ (1-42) infusion was significantly impaired behavioral memory, increased oxidative stress, decreased antioxidant enzyme and increased pro-inflammatory markers. Treatment of lupeol significantly restored Aβ (1-42) induced behavioral and biochemical abnormalities in rats brain. The findings of the present study suggest that lupeol act through multiple mechanisms and would be used to curb cognitive decline associated with neurodegenerative disorders of AD.

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Section: Isolation Of Lupeolsupporting

confidence: 85%

Lupeol Isolated from Betula alnoides Ameliorates Amyloid Beta Induced Neuronal Damage via Targeting Various Pathological Events and Alteration in Neurotransmitter Levels in Rat’s Brain

Kaundal¹,

Akhtar²,

Deshmukh³

2017

J Neurol Neurosci

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“…There is a widespread interest in the development of suitable models of AD. Several in vivo models have been established for testing drug candidates, most of the models attempting to mimic the lesions or symptoms in AD (Dodart and May 2005). In some experiments, amyloid peptides (Chacon et al 2004;Seabrook et al 2004) or other exogenous chemicals (Nivsarkar et al 2008) are injected into the brains of living mice or rats, while in others the cholinergic system (Nag and Tang 1998) is destroyed to reproduce lesions, neurotoxicity, or behavioral symptoms.…”

Section: Introductionmentioning

confidence: 99%

“…Acute or chronic injections of Ab or other exogenous chemicals in rodents allowed the creation of animal models showing several characteristics of AD, such as amyloid deposition or neurofibrillary tangles (Dodart and May 2005), but the injection procedure to brain regions, like hippocampus (Chacon et al 2004) or entorhinal cortex (Sipos et al 2007) is an invasive technique, and can induce inflammation, infection, and mortality. On the other hand, the diffusion of the chemicals or peptides from the injection sites is problematic and depends largely on the size and the solubility of the injected compound.…”

Section: Introductionmentioning

confidence: 99%

Intranasal Delivery of Human β-Amyloid Peptide in Rats: Effective Brain Targeting

et al. 2009

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(1) Intranasal administration is a non-invasive and effective way for the delivery of drugs to brain that circumvents the blood-brain barrier. The aims of the study were to test a nasal delivery system for human beta-amyloid (A beta) peptides, to measure the delivery of the peptides to brain regions, and to test their biological activity in rats. (2) A beta(1-42), in the form of a mixture of oligomers, protofibrils, and fibrils was dissolved in a nasal formulation containing hydrophobic, hydrophylic, and mucoadhesive components. The peptide solution was administered intranasally to rats as a single dose or in repeated doses. (3) Nasally injected A beta labeled with the blue fluorescent dye amino-methyl coumarinyl acetic acid (AMCA) could be detected by fluorescent microscopy in the olfactory bulb and frontal cortex. The concentration of the peptide was quantified by fluorescent spectroscopy, and a significant amount of AMCA-A beta peptide could be detected in the olfactory bulb. Unlabeled A beta also reached the olfactory bulb and frontal cortex of rats as evidenced by intense immunostaining. (4) In behavioral experiments, nasal A beta treatment did not affect anxiety levels (open-field test) and short-term memory (Y-maze test), but significantly impaired long-term spatial memory in the Morris water maze. The treatments did not result in A beta immunization. (5) The tested intranasal delivery system could successfully target a bioactive peptide into the central nervous system and provides a basis for developing a non-invasive and cost effective, new model to study amyloid-induced dysfunctions in the brain.

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“…Although Aβ in rodents has a slightly different amino acid sequence compared to human and monkey peptides, it can form fibrils [17] indicating that the lack of evident amyloid deposits in rodent brain is not due directly to the specific changes in its sequence but to other factors. Because of that, most animal models of AD use transgenic mice and rats, which express human AD-related proteins such as amyloid precursor protein (APP), presenilins (PS1 and PS2), and tau protein (for review see [18]). …”

Section: Introductionmentioning

confidence: 99%

Ontogenetic and Phylogenetic Approaches for Studying the Mechanisms of Cognitive Dysfunctions

Журавин¹,

Dubrovskaya²,

Туманова³

et al. 2018

Evolutionary Physiology and Biochemistry - Advances and Perspectives

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This chapter summarizes the phylogenetic and ontogenetic approaches for studying cognitive disorders such as Alzheimer's disease. It gives an extended example of evaluation of animal behavior and brain properties using an original model of prenatal hypoxia in rats by various physiological, behavioral, immunohistochemical, molecular biological, and biochemical techniques at different stages of postnatal development, which provide a better understanding of the pathological processes in the human brain during the development of neurodegeneration.

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Overview on Rodent Models of Alzheimer's Disease

Cited by 25 publications

References 138 publications

Lupeol Isolated from Betula alnoides Ameliorates Amyloid Beta Induced Neuronal Damage via Targeting Various Pathological Events and Alteration in Neurotransmitter Levels in Rat’s Brain

Lupeol Isolated from Betula alnoides Ameliorates Amyloid Beta Induced Neuronal Damage via Targeting Various Pathological Events and Alteration in Neurotransmitter Levels in Rat’s Brain

Intranasal Delivery of Human β-Amyloid Peptide in Rats: Effective Brain Targeting

Ontogenetic and Phylogenetic Approaches for Studying the Mechanisms of Cognitive Dysfunctions

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