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      Acetyl-L-Carnitine in Dementia and Other Cognitive Disorders: A Critical Update

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          Abstract

          Several studies explored the effects of acetyl-L-carnitine (ALC) in dementia, suggesting a role in slowing down cognitive decline. Nevertheless, in 2003 a systematic review concluded there was insufficient evidence to recommend a clinical use, although a meta-analysis in the same year showed a significant advantage for ALC for clinical scales and psychometric tests. Since then, other studies have been published; however, a critical review is still lacking. We provide an update of the studies on ALC in primary and secondary dementia, highlighting the current limitations and translational implications. Overall, the role of ALC in dementia is still under debate. The underlying mechanisms may include restoring of cell membranes and synaptic functioning, enhancing cholinergic activity, promoting mitochondrial energy metabolism, protecting against toxins, and exerting neurotrophic effects. The effects of ALC on the gut–liver–brain axis seem to identify the category of patients in which the new insights contribute most to the mechanisms of action of ALC, likely being the liver metabolism and the improvement of hepatic detoxifying mechanisms the primary targets. In this framework, our research group has dealt with this topic, focusing on the ALC-related cross-talk mechanisms. Further studies with homogeneous sample and longitudinal assessment are needed before a systematic clinical application.

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          The diagnosis and management of mild cognitive impairment: a clinical review.

          Cognitive decline is a common and feared aspect of aging. Mild cognitive impairment (MCI) is defined as the symptomatic predementia stage on the continuum of cognitive decline, characterized by objective impairment in cognition that is not severe enough to require help with usual activities of daily living.
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            Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain

            Recent evidence indicates that the nucleus basalis of Meynert, a distinct population of basal forebrain neurons, is a major source of cholinergic innervation of the cerebral cortex. Postmortem studies have previously demonstrated profound reduction in the presynaptic markers for cholinergic neurons in the cortex of patients with Alzheimer's disease and senile dementia of the Alzheimer's type. The results of this study show that neurons of the nucleus basalis of Meynert undergo a profound (greater than 75 percent) and selective degeneration in these patients and provide a pathological substrate of the cholinergic deficiency in their brains. Demonstration of selective degeneration of such neurons represents the first documentation of a loss of a transmitter-specific neuronal population in a major disorder of higher cortical function and, as such, points to a critical subcortical lesion in Alzheimer's patients.
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              Current and Future Treatments in Alzheimer Disease: An Update

              Disease-modifying treatment strategies for Alzheimer disease (AD) are still under extensive research. Nowadays, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance: 3 cholinesterase inhibitors and memantine. To block the progression of the disease, therapeutic agents are supposed to interfere with the pathogenic steps responsible for the clinical symptoms, classically including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation. Other underlying mechanisms are targeted by neuroprotective, anti-inflammatory, growth factor promotive, metabolic efficacious agents and stem cell therapies. Recent therapies have integrated multiple new features such as novel biomarkers, new neuropsychological outcomes, enrollment of earlier populations in the course of the disease, and innovative trial designs. In the near future different specific agents for every patient might be used in a “precision medicine” context, where aberrant biomarkers accompanied with a particular pattern of neuropsychological and neuroimaging findings could determine a specific treatment regimen within a customized therapeutic framework. In this review, we discuss potential disease-modifying therapies that are currently being studied and potential individualized therapeutic frameworks that can be proved beneficial for patients with AD.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                12 May 2020
                May 2020
                : 12
                : 5
                : 1389
                Affiliations
                [1 ]Department of Biomedical and Biotechnological Science, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy; manuela.pennisi@ 123456unict.it (M.P.); drfrancescofisicaro@ 123456gmail.com (F.F.); giulia.malaguarnera@ 123456live.it (G.M.)
                [2 ]Department of Surgery and Medical-Surgical Specialties, University of Catania, Via Santa Sofia 78, 95123 Catania, Italy
                [3 ]Department of Neurology IC, Oasi Research Institute-IRCCS, Via Conte Ruggero 73, 94018 Troina, Italy
                [4 ]Department of Neurology, Sant’Elia Hospital, Azienda Sanitaria Provinciale (ASP) Caltanissetta, Via Luigi Russo 6, 93100 Caltanissetta, Italy; m.cantone@ 123456asp.cl.it
                [5 ]Department of Medical and Surgical Sciences and Advanced Technologies, University of Catania, Via Santa Sofia 78, 95123 Catania, Italy; emanuele.damico@ 123456unict.it (E.D.); rbella@ 123456unict.it (R.B.)
                [6 ]Department of Neurology, Azienda Socio-Sanitaria Territoriale (ASST) Cremona, Viale Concordia 1, 26100 Cremona, Italy; valentina.puglisi@ 123456asst-cremona.it (V.P.); luisa.vinciguerra@ 123456asst-cremona.it (L.V.)
                [7 ]Department of Clinical and Experimental Medicine, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy; enzodante@ 123456email.it
                [8 ]Research Center “The Great Senescence”, University of Catania, Via Androne 83, 95124 Catania, Italy
                Author notes
                [* ]Correspondence: glanza@ 123456oasi.en.it ; Tel.: +39-095-3782448
                [†]

                Equally contributed to this work (in either order).

                Author information
                https://orcid.org/0000-0002-5659-662X
                https://orcid.org/0000-0002-9072-4971
                https://orcid.org/0000-0001-7494-9057
                https://orcid.org/0000-0002-1579-8807
                https://orcid.org/0000-0003-3655-4307
                Article
                nutrients-12-01389
                10.3390/nu12051389
                7284336
                32408706
                790d2f40-a743-492f-9a0a-9349ed2c0592
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 09 April 2020
                : 06 May 2020
                Categories
                Review

                Nutrition & Dietetics
                acetyl-l-carnitine,neurodegeneration,dementia,mild cognitive impairment,memory loss,biochemistry,neuroplasticity,hepatic encephalopathy,gut–liver–brain axis

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