Obovatol improves cognitive functions in animal models for Alzheimer’s disease

  title={Obovatol improves cognitive functions in animal models for Alzheimer’s disease},
  author={Dong Young Choi and Jae Woong Lee and Jin Peng and Young Jung Lee and Jin-Yi Han and Yeon Hee Lee and Im Seop Choi and Sang Bae Han and Jae-Kyung Jung and Woong Soo Lee and Seung-Ho Lee and Byoung‐Mog Kwon and Ki-Wan Oh and Jin Tae Hong},
  journal={Journal of Neurochemistry},
J. Neurochem. (2012) 120, 1048–1059. 

Antimalarial Drug Artemisinin Extenuates Amyloidogenesis and Neuroinflammation in APPswe/PS1dE9 Transgenic Mice via Inhibition of Nuclear Factor‐κB and NLRP3 Inflammasome Activation

The activation of nuclear factor‐kappa B and NLRP3 inflammasome is involved in neuroinflammation, which is closely linked to Alzheimer's disease (AD), and the impacts of artemisinin on AD have not been investigated.

Involvement of inflammation in Alzheimer’s disease pathogenesis and therapeutic potential of anti-inflammatory agents

Supportive evidence that neuroinflammation plays a critical role in AD development is focused on and putative therapeutic capacity of anti-inflammatory drugs for AD prevention or treatment is depicted.

Attenuation of scopolamine-induced cognitive dysfunction by obovatol

Mechanism studies exhibited that obovatol dose-dependently alleviated scopolamine-induced increase in Aβ generation and β-secretase activity in the cortex and hippocampus, which suggests that the natural compound could be a useful agent for the prevention of the development or progression of AD neurodegeneration.

Protective effects of the Sophorae Fructus on cognitive impairment and neuroinflammatory alteration in an Aβ1-42-infused Alzheimer’s disease mouse model

It is suggested that KH034 treatment improves cognitive function and inhibits amyloidogenesis by the prevention of neuroinflammation in Aβ1–42 –infused mice, and may be useful in the prevention and treatment of neurodegenerative disorders such as Alzheimer’s disease.

Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease

KH032 attenuated cognitive defificits in the Aβ1-42-infused mice by increasing BDNF expression and ERK1/2 and CREB phosphorylation and inhibiting neuronal loss and neuroinflflammatory response, suggesting that KH032 has therapeutic potential in neurodegenerative disorders such as AD.

Cognitive enhancers (nootropics). Part 3: drugs interacting with targets other than receptors or enzymes. disease-modifying drugs.

The review covers the evolution of research in this field over the last 25 years and proposes assigning drugs to 19 categories according to their mechanism(s) of action.

Neuroprotective role of antioxidant and pyranocarboxylic acid derivative against AlCl 3 induced Alzheimer's disease in rats

Neuroprotective role of antioxidant and pyranocarboxylic acid derivative against AlCl3 induced Alzheimer’s disease in rats Sarabjeet Singh, Ramandeep Singh, Ajay S. Kushwah, Gaurav Gupta Pharmacology

Ficus erecta Thunb. Leaves Ameliorate Cognitive Deficit and Neuronal Damage in a Mouse Model of Amyloid-β-Induced Alzheimer’s Disease

EEFE protects against cognitive deficit and neuronal damage in AD-like mice via activation of the CREB/BDNF signaling and upregulation of the inflammatory cytokines.

Paeoniflorin Atttenuates Amyloidogenesis and the Inflammatory Responses in a Transgenic Mouse Model of Alzheimer’s Disease

It is demonstrated that paeoniflorin exhibits neuroprotective effects in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice via inhibiting neuroinflammation mediated by the GSK-3β and NF-κB signaling pathways and nucleotide-binding domain-like receptor protein 3 inflammasome.



Obovatol attenuates microglia‐mediated neuroinflammation by modulating redox regulation

Obovatol isolated from the medicinal herb Magnolia obovata exhibits a variety of biological activities and its mechanism of action on microglial activation, neuro inflammation and neurodegeneration was investigated.

Neuroinflammation in Alzheimer's disease: are NSAIDs and selective COX-2 inhibitors the next line of therapy?

Empirical, preclinical, and clinical evidence evaluating the efficacy of various NSAIDs and selective COX-2 inhibitors in AD is outlined, and recent anecdotal data with the TNF-α inhibitor, etanercept, is reviewed.

Ibuprofen Suppresses Plaque Pathology and Inflammation in a Mouse Model for Alzheimer's Disease

The anti-inflammatory drug ibuprofen, which has been associated with reduced AD risk in human epidemiological studies, can significantly delay some forms of AD pathology, including amyloid deposition, when administered early in the disease course of a transgenic mouse model of AD.

Molecular basis of Alzheimer's disease

Since the physiological role of APP, presenilins, and apolipoprotein E in the central nervous system are not completely understood, their involvement in AD etiology remains speculative and new actors have to be found to explain sporadic cases and non-elucidated familial cases.

Increased expression of the amyloid precursor β‐secretase in Alzheimer's disease

The levels of the amyloid precursor protein C‐terminal fragment produced by β‐secretase to be increased by nearly twofold in Alzheimer's disease cortex is found.

Cyclooxygenase-2 inhibition improves amyloid-beta-mediated suppression of memory and synaptic plasticity.

It is reported that the selective inhibition of COX-2, but notCOX-1, acutely prevented the suppression of hippocampal long-term plasticity (LTP) by Abeta, and a third possible mechanism by which NSAIDs may protect against Alzheimer's disease is proposed, involving the blockade of a COx-2-mediated PGE2 response at synapses.

Anti-Inflammatory Drug Therapy Alters β-Amyloid Processing and Deposition in an Animal Model of Alzheimer's Disease

Data show that chronic NSAID treatment can reduce brain Aβ levels, amyloid plaque burden, and microglial activation in an animal model of Alzheimer's disease.