What Is The Role Of Calcium In The Body – Two weeks of time-restricted isocaloric feeding reduces hepatic inflammation without significant weight loss in obese mice with nonalcoholic fatty liver disease

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What Is The Role Of Calcium In The Body

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Drugs Affecting Calcium Levels And Bone Mineralization

Received: October 29, 2020 / Revised: November 23, 2020 / Accepted: November 26, 2020 / Published: December 1, 2020

Calcium signaling is essential for neuronal function, and its dysregulation has been linked to neurodegenerative diseases, including Alzheimer’s disease (AD). There is a close interconnection between calcium signaling and mitochondrial function. Increasing evidence in various models of AD indicates that calcium dyshomeostasis dramatically alters mitochondrial activity, which in turn drives neurodegeneration. This review discusses the potential pathogenic mechanisms by which calcium impairs mitochondrial function in Alzheimer’s disease, focusing on the effects of calcium on endoplasmic reticulum (ER)–mitochondrial communication, mitochondrial transport, oxidative stress, and protein homeostasis. This review also summarizes recent data that highlight the need to investigate the mechanisms underlying calcium-dependent mitochondrial dysfunction, while suggesting potential targets for modulating mitochondrial calcium levels in the treatment of neurodegenerative diseases such as Alzheimer’s disease.

In the face of a rapidly aging population, neurodegenerative disorders are expected to become an increasingly pressing health problem, increasing the urgency for effective treatment. Most neurological disorders are chronic and incurable, and their debilitating effects can last for decades. There are approximately 50 million people living with dementia worldwide, and this number is expected to reach 82 million by 2030 and 152 million by 2050 (WHO.int) [1]. Alzheimer’s disease (AD), the most common neurodegenerative disease [1], is the sixth leading cause of death [2]. In the United States alone, approximately 5 million people currently suffer from this disease, and this number is expected to triple by 2050 [2]. AD is characterized by gradual cognitive decline and memory loss, synaptic dysfunction, and neuronal death. Despite decades of research, there is no effective therapy for AD, and the cause of AD remains unclear, especially due to its complex etiology. The primary histopathological features of AD are neurofibrillary tangles composed of microtubule-associated protein tau and extracellular deposition of senile plaques composed of amyloid-beta (Abeta) peptides. Most research on AD has focused on examining the amyloid hypothesis, which posits that abnormal production of Abeta is the primary cause of AD and that all other dysfunctions observed in AD, including hyperphosphorylated tau tangles, are a consequence of Abeta neurotoxicity. Abeta plaques themselves have been shown to disrupt synaptic function and cause widespread neuronal death, particularly in the cortical and hippocampal regions of the brain, which are responsible for learning and memory [3]. In support of the claim that Abeta is the causative agent of AD, genetic mutations in the genes encoding presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP) that lead to almost all familial early-onset Alzheimer’s disease (FAD) ) cases, all are involved in processing by Abeta. Abeta peptides of various lengths are formed from APP by sequential cleavage by beta-secretase and gamma-secretase. Mutations in the genes encoding PSEN1 and PSEN2, which underlie approximately 70% of all familial cases of AD [4], form the catalytic component of the gamma-secretase complex. The main cause of AD is believed to be increased production of the more toxic, aggregation-prone species of Abeta42 compared to Abeta40, which results in the production of extracellular amyloid fibrils and plaques [3]. Therapeutic strategies to treat AD focus on reducing the burden of Abeta plaques by preventing Abeta production or promoting their clearance. However, gamma-secretase inhibitors have been clinically unsuccessful, and Abeta plaque burden is not strongly correlated with the onset or severity of dementia [5], prompting reconsideration of the amyloid hypothesis [6, 7, 8, 9]. There is also significant evidence that Abeta oligomers, as opposed to the more aggregated Abeta fibrils, are the main cytotoxic species and pathological agent of AD. This soluble form has been shown to damage synapses without the formation of Abeta plaques [10, 11]. Additionally, oligomeric Abeta isolated from AD patients was sufficient to cause synaptic dysfunction and memory loss in mice [12]. It is unclear whether selective targeting of Abeta oligomers will result in greater success in clinical trials. Indeed, the use of Abeta-targeted immunotherapies, which have been shown to bind to oligomeric Abeta with high affinity, has no effect on disease progression [8, 13]. Other studies have shown that overexpression of Abeta peptides in mice, simulating the Abeta pathology observed in AD, does not cause similar synaptic loss and memory impairment [14]. Moreover, in the absence of Abeta production, neurodegeneration may occur due to presenilin mutations [15, 16]. Mutations in other components of the gamma-secretase complex (APH-1, PEN-2, and nicastrin) are not associated with FAD, suggesting that APP and presenilin mutations do not cause FAD merely by altering Abeta production [17]. Moreover, many other symptoms (e.g. increased inflammation, altered calcium signaling, mitochondrial dysfunction, oxidative damage) appear to occur independently of any Abeta involvement, as they often precede Abeta plaque formation and are also more strongly correlated with cognitive decline [18 , 19 ] Taken together, this suggests that Abeta production is not necessarily a direct cause of AD and that additional pathological factors need to be investigated to develop effective therapies.

The link between calcium and Alzheimer’s disease was observed decades ago [20], but recent data support this hypothesis and strongly indicate a role for calcium in Alzheimer’s disease. The calcium hypothesis in AD states that disruptions in neuronal calcium signaling underlie not only the deposition of amyloid plaques but also a number of molecular changes within the neuron that cause neuronal dysfunction [21]. During neurotransmission, an increase in intracellular calcium due to membrane depolarization transmits the signal to the synapses. Calcium signaling in neurons is therefore crucial for neurotransmission and the maintenance of synaptic plasticity and the generation of long-term potentiation (LTP), which underlies learning and memory through the gradual strengthening of synapses [22, 23]. Calcium signaling also regulates neuronal metabolism and energy production, which is necessary to maintain synaptic transmission [24]. It is therefore not surprising that disruptions in calcium signaling have devastating consequences on neuronal function. Evidence for calcium dysregulation in AD was first found over 25 years ago in fibroblast cells isolated from AD patients, which showed increased calcium uptake by the endoplasmic reticulum (ER) and calcium release from the ER [25, 26]. Further studies in mouse models of AD confirmed the ubiquitous involvement of calcium dysregulation in AD, linking it to memory loss and increased toxicity of Abeta peptides [27, 28, 29]. Other studies have shown that elevated ER or cytoplasmic calcium levels increase Abeta production by triggering APP and tau phosphorylation, indicating that intracellular calcium dysregulation exacerbates amyloidosis and tau pathology [30, 31]. Emilsson and Jazin also showed that the mRNA expression of genes involved in calcium regulation is altered in the brains of AD patients [32]. The results of this study further suggest that ER calcium channel activity is increased in Alzheimer’s disease [32].

Pdf) Role Of Calcium During Pregnancy: Maternal And Fetal Needs

Many familial AD PSEN mutations are also associated with dysregulated calcium signaling [33]. In addition to the role of PSEN1/2 as the catalytic subunit of gamma-secretase, PSEN1/2 regulates calcium storage in the ER, a function that is notably independent of gamma-secretase, demonstrating that the effects of PSEN1 and PSEN2 on neuronal function extend beyond the Abeta generation [34, 35]. PSEN1/2 are transmembrane proteins present on most endomembranes but predominant on the ER membrane, where they have been found to physically interact with ER calcium channels, including the two main calcium release channels in the ER, inositol 1, 4, 5-triphosphate receptors ( IP

Rs) and ryanodine receptors (RyR) [28, 36, 37]. Consistent with this, mice carrying FAD mutations show altered activity of both IPs

Rs and RyRs. Presenilin mutations have been documented to increase RyR and IP expression or sensitivity

R-mediated calcium release in response to various agonists [28, 36, 38, 39, 40]. PSEN1 loss of function

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