Life at Low Reynolds Number

Almond, hazelnut and walnut, three nuts for neuroprotection in Alzheimer's disease: A neuropharmacological review of their bioactive constituents.

Bone metastasis is the leading cause of death in prostate cancer patients, for which there is currently no effective treatment. Since the bone microenvironment plays an important role in this process, attentions have been directed to the interactions between cancer cells and the bone microenvironment, including osteoclasts, osteoblasts, and bone stromal cells. Here, we explained the mechanism of interactions between prostate cancer cells and metastasis-associated cells within the bone microenvironment and further discussed the recent advances in targeted therapy of prostate cancer bone metastasis. This review also summarized the effects of bone microenvironment on prostate cancer metastasis and the related mechanisms, and provides insights for future prostate cancer metastasis studies.

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Interactions between cancer cells and bone microenvironment promote bone metastasis in prostate cancer

Development of nanomaterials for bone-targeted drug delivery

The early detection and thus treatment of breast cancer bone metastasis remain a big challenge clinically. As the most abundant cells within bone tissue, osteocytes have been found to manipulate the activity of early cancer bone metastasis by its crosstalk with cancer cells and osteoclasts. However, conventional bone-targeting nanomedicine has limited bone-lesion specificity and ignores the vital role of osteocytes during breast cancer bone metastasis. Also, it lacks detailed insight into the therapeutic mechanisms, which hinders the following translational practice. Previously, we have shown that a combination of zoledronic acid (ZA) and plumbagin (PL) synergistically alleviates cancer-induced bone destruction. Herein, we further develop a pH-responsive bone-targeting drug delivery system, i.e., the ZA-anchored bimodal mesoporous slica covered gadolinium(III) upconversion nanoparticles loaded with PL, to detect and treat bone metastasis sensitively and specifically at an early stage. This multifunctional...

Targeting Osteocytes to Attenuate Early Breast Cancer Bone Metastasis by Theranostic Upconversion Nanoparticles with Responsive Plumbagin Release

Alzheimer's disease (AD) is the foremost type of dementia that afflicts considerable morbidity and mortality in aged population. Several transcription molecules, pathways, and molecular mechanisms such as oxidative stress, inflammation, autophagy, and immune system interact in a multifaceted way that disrupt physiological processes (cell growth, differentiation, survival, lipid and energy metabolism, endocytosis) leading to apoptosis, tauopathy, β-amyloidopathy, neuron, and synapse loss, which play an important role in AD pathophysiology. Despite of stupendous advancements in pathogenic mechanisms, treatment of AD is still a nightmare in the field of medicine. There is compelling urgency to find not only symptomatic but effective disease-modifying therapies. Recently, phosphoinositide 3-kinase (PI3K) and Akt are identified as a pathway triggered by diverse stimuli, including insulin, growth factors, cytokines, and cellular stress, that link amyloid-β, neurofibrillary tangles, and brain atrophy. The present review aims to explore and analyze the role of PI3K-Akt pathway in AD and agents which may modulate Akt and have therapeutic prospects in AD. The literature was researched using keywords "PI3K-Akt" and "Alzheimer's disease" from PubMed, Web of Science, Bentham, Science Direct, Springer Nature, Scopus, and Google Scholar databases including books. Articles published from 1992 to 2021 were prioritized and analyzed for their strengths and limitations, and most appropriate ones were selected for the purpose of review. PI3K-Akt pathway regulates various biological processes such as cell proliferation, motility, growth, survival, and metabolic functions, and inhibits many neurotoxic mechanisms. Furthermore, experimental data indicate that PI3K-Akt signaling might be an important therapeutic target in treatment of AD.

Implications of Phosphoinositide 3-Kinase-Akt (PI3K-Akt) Pathway in the Pathogenesis of Alzheimer's Disease

Cancer becomes the leading cause of deaths worldwide, including breast cancer, prostate cancer and lung cancer that preferentially metastasize to bone and bone marrow. Bisphosphonates (BPs) have been used successfully for many years to reduce the skeletal complications related with the benign and malignant bone diseases that are characterized by enhanced osteoclastic bone resorption. Nitrogen-containing bisphosphonates (N-BPs) have also been demonstrated to exhibit direct anti-tumour effects. BPs binds avidly to the bone matrix, and released from matrix during bone resorption process, BPs are internalized by the osteoclasts where they interfere with biochemical pathways and induce osteoclast apoptosis. BPs also antagonizes the production of osteoclast and promotes the osteoblasts proliferation. Currently, Zoledronic acid is widely used as one of the BP having high bone specificity and potential to inhibit the osteoclast-mediated bone resorption. In addition to inhibition of cell multiplication and initiation of apoptosis in cultured cancer cells, they also interfere with adhesion of cancer cells to the bone matrix and inhibit cell migration and invasion. Pathophysiology and current target therapies like conjugate of BPs with liposomes, nanoparticle used for the treatment of bone cancer is reviewed in this article along with the use of different BPs.

The critical role of bisphosphonates to target bone cancer metastasis: an overview.

Mitochondrial abnormalities and redox imbalance are major pathogenic factors in progression of Huntington’s disease (HD), manifested clinically by affective, motor, cognitive, and psychiatric incompetence Antioxidants behold much promise in mitigation of several pathological facets in HD Ellagic acid (EA) is a naturally derived polyphenol acknowledged for potent neuroprotective abilities that enabled its significance amongst popular brain tonics The present study is aimed to examine the outcome of EA pre-treatment in 3-nitropropionic acid (3-NP) rat prototype of HD Separate rat groups were pre-treated with EA (25, 50, and 100 mg/kg, po) for 21 days and 3-NP (10 mg/kg, ip) was given for 14 days alongside to induce symptoms of HD The physical/motor functions (narrow beam paradigm, footprint study, hanging-wire assessment) and cognitive abilities using elevated plus maze and novel object recognition task were evaluated Entire brain was isolated and succinate dehydrogenase activity and parameters of oxido-nitrosative stress were assessed in mitochondrial fraction 3-NP accrued oxido-nitrosative stress and significant decrease in succinate dehydrogenase activity caused motor and cognitive deficits in rats EA pre-treatment resurrected succinate dehydrogenase activity in 3-NP treated rats that indicated preservation of mitochondrial function A significant decrease in thiobarbituric acid reactive substances and nitrite levels and increase in glutathione and catalase activity by EA in 3-NP treated rats was noted EA protected the rats against 3-NP triggered cognitive insufficiency and motor disturbances It can be inferred that ellagic acid protects against 3-NP induced mitochondrial dysfunction and oxido-nitrosative stress in the brain EA supplements or nutraceuticals might possess protective potential against symptoms of HD

Ellagic acid prevents 3-nitropropionic acid induced symptoms of Huntington's disease.

Arbutin attenuates monosodium L-glutamate induced neurotoxicity and cognitive dysfunction in rats.

Neuroprotective effects of theobromine in transient global cerebral ischemia-reperfusion rat model.

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