Re-thinking the Etiological Framework of Neurodegeneration

Castillo, Ximena; Castro-Obregón, Susana; Gutiérrez-Becker, Benjamín; Gutiérrez‐Ospina, Gabriel; Karalis, Nikolaos; Khalil, Ahmed A.; Lopez-Noguerola, José Sócrates; Rodríguez, Liliana Lozano; Martínez‐Martínez, Eduardo; Pérez-Cruz, Claudia; Pérez-Velázquez, Judith; Piña, Ana Luisa; Rubio, Karla; Garcia, Hector P. Salazar; Syeda, Tauqeerunnisa; Vanoye-Carlo, América; Villringer, Arno; Winek, Katarzyna; Zille, Marietta

doi:10.3389/fnins.2019.00728

Cited by 60 publications

(33 citation statements)

References 337 publications

(379 reference statements)

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“…The increase in serum ADPN in AD may reflect systemic and compensatory mechanism against neurodegeneration [51]. However, this compensatory mechanism is limited.…”

Section: Adiponectin and Alzheimer Disease (Ad)mentioning

confidence: 99%

Adiponectin and Cognitive Decline

Rizzo

Fasano

Paolisso

2020

IJMS

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Adiponectin (ADPN) is a plasma protein secreted by adipose tissue showing pleiotropic effects with anti-diabetic, anti-atherogenic, and anti-inflammatory properties. Initially, it was thought that the main role was only the metabolism control. Later, ADPN receptors were also found in the central nervous system (CNS). In fact, the receptors AdipoR1 and AdipoR2 are expressed in various areas of the brain, including the hypothalamus, hippocampus, and cortex. While AdipoR1 regulates insulin sensitivity through the activation of the AMP-activated protein kinase (AMPK) pathway, AdipoR2 stimulates the neural plasticity through the activation of the peroxisome proliferator-activated receptor alpha (PPARα) pathway that inhibits inflammation and oxidative stress. Overall, based on its central and peripheral actions, ADPN appears to have neuroprotective effects by reducing inflammatory markers, such as C-reactive protein (PCR), interleukin 6 (IL6), and Tumor Necrosis Factor a (TNFa). Conversely, high levels of inflammatory cascade factors appear to inhibit the production of ADPN, suggesting bidirectional modulation. In addition, ADPN appears to have insulin-sensitizing action. It is known that a reduction in insulin signaling is associated with cognitive impairment. Based on this, it is of great interest to investigate the mechanism of restoration of the insulin signal in the brain as an action of ADPN, because it is useful for testing a possible pharmacological treatment for the improvement of cognitive decline. Anyway, if ADPN regulates neuronal functioning and cognitive performances by the glycemic metabolic system remains poorly explored. Moreover, although the mechanism is still unclear, women compared to men have a doubled risk of developing cognitive decline. Several studies have also supported that during the menopausal transition, the estrogen reduction can adversely affect the brain, in particular, verbal memory and verbal fluency. During the postmenopausal period, in obese and insulin-resistant individuals, ADPN serum levels are significantly reduced. Our recent study has evaluated the relationship between plasma ADPN levels and cognitive performances in menopausal women. Thus, the aim of this review is to summarize both the mechanisms and the effects of ADPN in the central nervous system and the relationship between plasma ADPN levels and cognitive performances, also in menopausal women.

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“…The increase in serum ADPN in AD may reflect systemic and compensatory mechanism against neurodegeneration [51]. However, this compensatory mechanism is limited.…”

Section: Adiponectin and Alzheimer Disease (Ad)mentioning

confidence: 99%

Adiponectin and Cognitive Decline

Rizzo

Fasano

Paolisso

2020

IJMS

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“…Treatments for neurodegenerative diseases result in great economic costs, in terms of medical and long-term care. The incidence of neurodegenerative diseases is also expected to grow, and become the second leading cause of death after cardiovascular disease [6].…”

Section: Introductionmentioning

confidence: 99%

An Overview of Crucial Dietary Substances and Their Modes of Action for Prevention of Neurodegenerative Diseases

Pogačnik

Ota

Ulrih

2020

Cells

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Neurodegenerative diseases, namely Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis, Huntington’s disease, and multiple sclerosis are becoming one of the main health concerns due to the increasing aging of the world’s population. These diseases often share the same biological mechanisms, including neuroinflammation, oxidative stress, and/or protein fibrillation. Recently, there have been many studies published pointing out the possibilities to reduce and postpone the clinical manifestation of these deadly diseases through lifelong consumption of some crucial dietary substances, among which phytochemicals (e.g., polyphenols) and endogenous substances (e.g., acetyl-L-carnitine, coenzyme Q10, n-3 poysaturated fatty acids) showed the most promising results. Another important issue that has been pointed out recently is the availability of these substances to the central nervous system, where they have to be present in high enough concentrations in order to exhibit their neuroprotective properties. As so, such the aim of this review is to summarize the recent findings regarding neuroprotective substances, their mechanisms of action, as well as to point out therapeutic considerations, including their bioavailability and safety for humans.

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“…The burden of neurodegenerative diseases has significantly increased worldwide over the past 25 years, mostly due to incremental increases in the population numbers, population ageing and to the environmental stress associated to contemporary societies [1][2][3]. These diseases have become the leading cause of disability and death in developed countries and, in spite of decades of research, there is no way to cure them or slow down their progression [4]. Neurodegenerative diseases include Alzheimer's, amyotrophic lateral sclerosis, Huntington's, Lewy body disease and Parkinson's, among others.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection or Neurotoxicity of Illicit Drugs on Parkinson’s Disease

Ferreira

Almeida²,

Tenreiro

et al. 2020

Life

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Parkinson’s Disease (PD) is currently the most rapid growing neurodegenerative disease and over the past generation, its global burden has more than doubled. The onset of PD can arise due to environmental, sporadic or genetic factors. Nevertheless, most PD cases have an unknown etiology. Chemicals, such as the anthropogenic pollutant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and amphetamine-type stimulants, have been associated with the onset of PD. Conversely, cannabinoids have been associated with the treatment of the symptoms’. PD and medical cannabis is currently under the spotlight, and research to find its benefits on PD is on-going worldwide. However, the described clinical applications and safety of pharmacotherapy with cannabis products are yet to be fully supported by scientific evidence. Furthermore, the novel psychoactive substances are currently a popular alternative to classical drugs of abuse, representing an unknown health hazard for young adults who may develop PD later in their lifetime. This review addresses the neurotoxic and neuroprotective impact of illicit substance consumption in PD, presenting clinical evidence and molecular and cellular mechanisms of this association. This research area is utterly important for contemporary society since illicit drugs’ legalization is under discussion which may have consequences both for the onset of PD and for the treatment of its symptoms.

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Re-thinking the Etiological Framework of Neurodegeneration

Cited by 60 publications

References 337 publications

Adiponectin and Cognitive Decline

Adiponectin and Cognitive Decline

An Overview of Crucial Dietary Substances and Their Modes of Action for Prevention of Neurodegenerative Diseases

Neuroprotection or Neurotoxicity of Illicit Drugs on Parkinson’s Disease

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