China
Africa
Explore chapters and articles related to this topic
Role of Vitamin D and Antioxidant Functional Foods in the Prevention and Treatment of Alzheimer’s Disease Pathology
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Polyphenols are plant metabolites that can be obtained by the consumption of fruits, vegetables, and legumes, as well as tea, coffee, and wine. They have been considered potent inhibitors of beta-amyloid aggregation (Phan et al., 2019). Examples of these types are flavonoids and hydroxybenzoic acid derivatives (such as protocatechuic and gallic acids). Flavonoids are among the largest types of potentially beneficial active plant substances. They have variable phenolic structures and are abundant in fruits and vegetables, as well as other plant-derived foods. Important subclasses relevant for AD include flavanones, flavonols, and isoflavonoids (Panche, Diwan, & Chandra, 2016). Some of these substances, such as carboxy acid derivatives with triterpenoid or anthraquinoid portions, have structural features that interact in the Aβ2 dimer that are considered anti-aggregation properties (Murakami & Irie, 2019).
Pea
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Alzheimer disease (AD) is characterized by beta amyloid plaques, gliosis, and tau protein hyperphosphorylation leading to cognitive deficits in those affected. In an animal study by Scuderi et al.,20 beta amyloid was administered to the hippocampus of rats followed by PEA and the PPAR-α antagonist GW6471. The investigators found that PEA administration was correlated with a reduction in amnestic and cognitive deficits in the AD model rats. These results show a possible therapeutic option for AD patients for the improvement in cognitive deficits as well as disease progression.
Phytotherapeutic Potential For the Treatment of Alzheimer’s Disease
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
Muhammad Akram, Atanu Bhattacharjee, Naveed Munir, Naheed Akhter, Fozia Anjum, Abida Parveen, Samreen Gul Khan, Muhammad Daniyal, Muhammad Riaz, Fahad Said Khan, Rumaisa Ansari, Umme Laila
Amyloid is basically an insoluble form of protein, that is formed as a result of abnormal folding of polypeptides which are normally present. The precursor of amyloid is called Beta-Amyloid Precursor Protein (βAPP) that ultimately gives rise to amyloid proteins (Yuhai Zhao, 2014).
The aquaporin-4 water channel and updates on its potential as a drug target for Alzheimer’s disease
Published in Expert Opinion on Therapeutic Targets, 2023
Bret Silverglate, Xiaoyi Gao, Hannah P. Lee, Peter Maliha, George T. Grossberg
Alzheimer’s disease (AD) is the most common cognitive disorder in older adults. AD pathogenesis has long been associated with the formation of amyloid plaques and neurofibrillary tangles (NFTs). Amyloid plaques have detrimental effects on synaptic function and are composed of beta-amyloid proteins, which originate from amyloid precursor protein (APP). The insoluble NFTs consist of hyperphosphorylated tau and are also neurotoxic. Aquaporin channels (AQPs) are transmembrane proteins that function as bidirectional water and small solute channels. There are 13 classes of AQPs expressed in humans (AQPs 0–12). AQP4 channels expressed in human brain tissue are vital in clearing interstitial solutes, metabolic products, and protein aggregates (including the Aβ and hyperphosphorylated tau proteins mentioned above) from the brain via the glymphatic system, thus raising interest in its possible contribution to AD pathogenesis, and, importantly, in its potential pharmacologic targeting as treatment of AD [1,2].
Red-light radiation: does it enhance memory by increasing hippocampal LRP-1 and TRPA-1 genes expression?
Published in International Journal of Radiation Biology, 2023
Saereh Haghjoo, Mojtaba Hedayati Ch, Mohammad Rostampour, Behrooz Khakpour-Taleghani
Dementia is a broad term used to describe several progressive neurological diseases which mainly affect cognitive, behavioral, and memory performances. Alzheimer’s disease (AD) is the most common type accounts for 60–70% of dementia cases (Zhang et al. 2021). Although the underlying mechanism of age-related neurogenic disease-AD is still unknown, we know that it causes neuronal defects via accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles especially in the hippocampus and cortex (Ferreira et al. 2021). In addition, beta-amyloid accumulation activates astrocytes and microglia which lead to neuronal death due to the release of inflammatory factors (Wang et al. 2016). Furthermore, it has been identified that the beta-amyloid peptide is one of the main causative factors of mitochondrial dysfunction and oxidative stress. Free radicals that are connected with oxidative stress cause oxidative damage in the brain which leads to neurodegenerative diseases such as AD (Butterfield and Mattson 2020; Dasdag et al. 2020). Pituitary gland hormone, melatonin plays as a neuroprotective agent and its receptors are mainly expressed in astrocytes and microglia. Melatonin activates several signaling pathways which augment amyloid-beta (Aβ) clearance rate and reduce its production. Also, due to its electron transfer ability, it can eliminate free radicals directly (Roy et al. 2021).
Cortical hyperexcitability and plasticity in Alzheimer’s disease: developments in understanding and management
Published in Expert Review of Neurotherapeutics, 2022
Mehdi A. J van den Bos, Parvathi Menon, Steve Vucic
Pathologically, AD is characterized by extracellular deposits of beta-amyloid plaque and intraneuronal hyperphosphorylated tau which form deposits/neurofibrillary tangles (NFTs) leading to neurodegeneration[8]. Cholinergic[9], glutamatergic[10] and GABAergic neurons[7,11] are vulnerable to the effects of NFTs and Beta-amyloid plaque, and contribute to cortical hyperexcitability, a key step in neurodegeneration. An increase in neuronal activity can be provoked by the presence of beta-amyloid[12]. In turn chronic neuronal hyperactivity may drive the progressive accumulation of beta-amyloid[13] leading to a vicious cycle. In a similar manner neuronal hyperactivity can increase and perpetuate Tau pathology[14]. GABAergic interneurons exert inhibitory tone critical for maintaining the balance of cortical excitability. Beta-amyloid plaque has been shown to have impair GABAergic neuron function though downregulation of postsynaptic GABAA receptors[15] with consequent net hyperexcitability.