Dendrimers: A Neuroprotective Lead in Alzheimer Disease: A Review on
                    its Synthetic approach and Applications

Singh, Aditya; Ansari, Valeed Ahmad; Mahmood, Tarique; Ahsan, Farogh; Wasim, Rufaida

doi:10.1055/a-1886-3208

Cited by 10 publications

(8 citation statements)

References 47 publications

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“…For an impairment to meet the diagnostic criteria, it must be severe enough to interfere with daily activities or degrade from a higher level of function. It is necessary to rule out further treatable or reversible causes of cognitive deterioration [32,33].…”

Section: Microglia In Dementia and Cognitive Impairmentmentioning

confidence: 99%

Receptor for Advanced Glycation End Products: Dementia and Cognitive Impairment

et al. 2023

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The pathophysiological processes of dementia and cognitive impairment are linked to advanced glycation end products (AGEs) and their receptor (RAGE).The neurofibrillary tangles (NFTs) of abnormally hyperphosphorylated tau protein and senile plaques (SPs), which are brought on by amyloid beta (Aβ) deposition, are the hallmarks of Alzheimer’s disease (AD), a progressive neurodegenerative condition. Advanced glycation end products that are produced as a result of vascular dysfunction are bound by the receptor for advanced glycation end products (RAGE). Dementia and cognitive impairment could develop when RAGE binds to Aβ and produces reactive oxygen species, aggravating Aβ buildup and ultimately resulting in SPs and NFTs. RAGE could be a more powerful biomarker than Aβ because it is implicated in early AD. The resident immune cells in the brain known as microglia are essential for healthy brain function. Microglia is prominent in the amyloid plaques’ outside border as well as their central region in Alzheimer’s disease. Microglial cells, in the opinion of some authors, actively contribute to the formation of amyloid plaques. In this review, we first discuss the early diagnosis of dementia and cognitive impairment, and then detail the interaction between RAGE and Aβ and Tau that is necessary to cause dementia and cognitive impairment pathology, and it is anticipated that the creation of RAGE probes will help in the diagnosis and treatment of dementia and cognitive impairment.

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Section: Microglia In Dementia and Cognitive Impairmentmentioning

confidence: 99%

Receptor for Advanced Glycation End Products: Dementia and Cognitive Impairment

et al. 2023

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“…PLL inhibits tumor development by destroying necrosis and stimulating apoptosis. This contributes to the non-toxic effect PLL dendrimers have on healthy cells, bringing their therapeutic potential to the level of marketed anti-angiogenic drugs ( Ryan et al, 2013 ; Singh et al, 2022 ). A DOX-loaded PLL dendrimer coupled mainly with folate was synthesised by Jain and colleagues.…”

Section: Application Of Dendrimers As Drug Delivery Systems For the B...mentioning

confidence: 99%

Dendrimer: An update on recent developments and future opportunities for the brain tumors diagnosis and treatment

et al. 2023

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A brain tumor is an uncontrolled cell proliferation, a mass of tissue composed of cells that grow and divide abnormally and appear to be uncontrollable by the processes that normally control normal cells. Approximately 25,690 primary malignant brain tumors are discovered each year, 70% of which originate in glial cells. It has been observed that the blood-brain barrier (BBB) limits the distribution of drugs into the tumour environment, which complicates the oncological therapy of malignant brain tumours. Numerous studies have found that nanocarriers have demonstrated significant therapeutic efficacy in brain diseases. This review, based on a non-systematic search of the existing literature, provides an update on the existing knowledge of the types of dendrimers, synthesis methods, and mechanisms of action in relation to brain tumours. It also discusses the use of dendrimers in the diagnosis and treatment of brain tumours and the future possibilities of dendrimers. Dendrimers are of particular interest in the diagnosis and treatment of brain tumours because they can transport biochemical agents across the BBB to the tumour and into the brain after systemic administration. Dendrimers are being used to develop novel therapeutics such as prolonged release of drugs, immunotherapy, and antineoplastic effects. The use of PAMAM, PPI, PLL and surface engineered dendrimers has proven revolutionary in the effective diagnosis and treatment of brain tumours.

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“…Tau hyperphosphorylation and aggregation reduce the surface trafficking of APP, which exacerbates NFTs and contributes to toxic neuronal iron build-up, creating a vicious cycle. In fact, in a transient middle cerebral artery occlusion (MCAO) rat model, the tau-mediated APP pathway reduces iron-mediated neurotoxicity to prevent ferroptotic damage [18]. As a result, one major mechanism of neuronal injury and death is ROS production that is mediated by iron and tau as per ▶Fig.…”

Section: Role Of Ferritin In Ad Pathology Mechanismmentioning

confidence: 99%

Ferroptosis Signaling Pathways: Alzheimer's Disease

Maheshwari

2023

Horm Metab Res

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The involvements of iron metabolism, lipid peroxidation, and oxidative stress in Alzheimer's disease (AD) development have recently received a lot of attention. We also observe that these pathogenic occurrences play a key role in regulating ferroptosis, a unique regulatory cell death that is iron-dependent, oxidative, and non-apoptotic. Iron is a crucial component that makes up a subunit of the oxidase responsible for lipid peroxidation. A family of non-heme iron enzymes known as lipoxygenases (LOXs) can cause ferroptosis by oxidising polyunsaturated fatty acids in cellular membranes (PUFAs). Toxic lipid hydroperoxides are produced in large part by the iron in LOX active sites. Deferoxamine and deferiprone, two iron chelators, could also treat ferroptosis by eliminating the crucial catalytic iron from LOXs. Phospholipids containing polyunsaturated fatty acids are the main substrates of lipid peroxidation in ferroptosis, which is favourably controlled by enzymes like ACSL4, LPCAT3, ALOXs, or POR. Selective stimulation of autophagic degradation pathways leads to an increase in iron accumulation and lipid peroxidation, which promotes ferroptosis. We highlighted recent advancements in our understanding of ferroptosis signaling routes in this study. One form of regulated necrotic cell death known as ferroptosis has been linked to a number of diseases, including cancer, neurological disorders, and ischemia/reperfusion injury. Cerebrospinal fluid (CSF) ferritin may be a good indicator of the amount of iron in the brain because it is the main protein that stores iron.

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Dendrimers: A Neuroprotective Lead in Alzheimer Disease: A Review on its Synthetic approach and Applications

Cited by 10 publications

References 47 publications

Receptor for Advanced Glycation End Products: Dementia and Cognitive Impairment

Receptor for Advanced Glycation End Products: Dementia and Cognitive Impairment

Dendrimer: An update on recent developments and future opportunities for the brain tumors diagnosis and treatment

Ferroptosis Signaling Pathways: Alzheimer's Disease

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