Special Issue “Pathophysiology and Treatment of Alzheimer’s Disease”
1. Introduction
2. Discussion
Conflicts of Interest
References
- Fessel, J. Amyloid is essential but insufficient for Alzheimer causation: Addition of subcellular cofactors is required for dementia. Int. J. Geriatr. Psychiatry 2018, 33, e14–e21. [Google Scholar] [CrossRef] [PubMed]
- Fessel, J. Cure of Alzheimer’s Dementia Requires Addressing All of the Affected Brain Cell Types. J. Clin. Med. 2023, 12, 2049. [Google Scholar] [CrossRef] [PubMed]
- Sarkar, S.; Floto, R.A.; Berger, Z.; Imarisio, S.; Cordenier, A.; Pasco, M.; Cook, L.J.; Rubinsztein, D.C. Lithium induces autophagy by inhibiting inositol monophosphatase. J. Cell Biol. 2005, 170, 1101–1111. [Google Scholar] [CrossRef] [PubMed]
- Nie, D.; Peng, Y.; Li, M.; Liu, X.; Zhu, M.; Ye, L. Lithium chloride (LiCl) induced autophagy and downregulated expression of transforming growth factor β-induced protein (TGFBI) in granular corneal dystrophy. Exp. Eye Res. 2018, 173, 44–50. [Google Scholar] [CrossRef] [PubMed]
- Liang, G.; Anchipolovsky, S.; Zhang, R.; Das, I.; Ayala, B.; Xu, X.; Tsai, L.H.; Wei, H. Lithium protects against ApoE4 mediated calcium dysregulation and mitochondrial dysfunction and cell damage in iPSCs from a sporadic Alzheimer’s disease patient. Alzheimer’s Dement. 2023, 19, e082765. [Google Scholar] [CrossRef]
- McCarthy, M.J.; Nievergelt, C.M.; Kelsoe, J.R.; Welsh, D.K. A survey of genomic studies supports association of circadian clock genes with bipolar disorder spectrum illnesses and lithium response. PLoS ONE 2012, 7, e32091. [Google Scholar] [CrossRef] [PubMed]
- Xu, N.; Shinohara, K.; Saunders, K.E.; Geddes, J.R.; Cipriani, A. Effect of lithium on circadian rhythm in bipolar disorder: A systematic review and meta-analysis. Bipolar Disord. 2021, 23, 445–453. [Google Scholar] [CrossRef] [PubMed]
- Undurraga, J.; Sim, K.; Tondo, L.; Gorodischer, A.; Azua, E.; Tay, K.H.; Tan, D.; Baldessarini, R.J. Lithium treatment for unipolar major depressive disorder: Systematic review. J. Psychopharm. 2019, 33, 167–176. [Google Scholar] [CrossRef]
- Hu, M.; Wu, H.; Chao, C. Assisting effects of lithium on hypoglycemic treatment in patients with diabetes. Biol. Trace Elem. Res. 1997, 60, 131–137. [Google Scholar] [CrossRef]
- Marie-Claire, C.; Etain, B.; Bellivier, F. Mini review: Recent advances on epigenetic effects of lithium. Neurosci. Lett. 2021, 761, 136116. [Google Scholar] [CrossRef]
- Boufidou, F.; Nikolaou, C.; Alevizos, B.; Liappas, I.A.; Christodoulou, G.N. Cytokine production in bipolar affective disorder patients under lithium treatment. J. Affect. Disord. 2004, 82, 309–313. [Google Scholar] [CrossRef] [PubMed]
- Campbell, I.H.; Campbell, H.; Smith, D.J. Insulin signaling as a therapeutic mechanism of lithium in bipolar disorder. Transl. Psychiatry 2022, 12, 350. [Google Scholar] [CrossRef] [PubMed]
- Maurer, I.C.; Schippel, P.; Volz, H.P. Lithium-induced enhancement of mitochondrial oxidative phosphorylation in human brain tissue. Bipolar Disord. 2009, 11, 515–522. [Google Scholar] [CrossRef] [PubMed]
- De-Paula, V.J.; Gattaz, W.F.; Forlenza, O.V. Long-term lithium treatment increases intracellular and extracellular brain-derived neurotrophic factor (BDNF) in cortical and hippocampal neurons at subtherapeutic concentrations. Bipolar Disord. 2016, 18, 692–695. [Google Scholar] [CrossRef] [PubMed]
- Palmos, A.B.; Duarte, R.R.; Smeeth, D.M.; Hedges, E.C.; Nixon, D.F.; Thuret, S.; Powell, T.R. Lithium treatment and human hippocampal neurogenesis. Transl. Psychiatry 2021, 11, 555. [Google Scholar] [CrossRef] [PubMed]
- Valentín, A.; García-Seoane, J.; Colino, A. Lithium enhances synaptic transmission in neonatal rat hippocampus. Neuroscience 1997, 78, 385–391. [Google Scholar] [CrossRef] [PubMed]
- Lan, C.C.; Liu, C.C.; Lin, C.H.; Lan, T.Y.; McInnis, M.G.; Chan, C.H.; Lan, T.H. A reduced risk of stroke with lithium exposure in bipolar disorder: A population-based retrospective cohort study. Bipolar Disord. 2015, 17, 705–714. [Google Scholar] [CrossRef]
- Chen, R.-H.; Ding, W.V.; McCormick, F. Wnt signaling to β-catenin involves two interactive components: Glycogen synthase kinase-3β inhibition and activation of protein kinase C. J. Biol. Chem. 2000, 275, 17894–17899. [Google Scholar] [CrossRef]
- Wexler, E.; Geschwind, D.; Palmer, T. Lithium regulates adult hippocampal progenitor development through canonical Wnt pathway activation. Mol. Psychiatry 2008, 13, 285–292. [Google Scholar] [CrossRef]
- Su, Y.; Ryder, J.; Li, B.; Wu, X.; Fox, N.; Solenberg, P.; Brune, K.; Paul, S.; Zhou, Y.; Liu, F. Lithium, a Common Drug for Bipolar Disorder Treatment, Regulates Amyloid-β Precursor Protein Processing. Biochemistry 2004, 43, 6899–6908. [Google Scholar] [CrossRef]
- Zhang, X.; Heng, X.; Li, T.; Li, L.; Yang, D.; Zhang, X.; Du, Y.; Doody, R.S.; Le, W. Long-term treatment with lithium alleviates memory deficits and reduces amyloid-β production in an aged Alzheimer’s disease transgenic mouse model. J. Alzheimer’s Dis. 2011, 24, 739–749. [Google Scholar] [CrossRef]
- Caccamo, A.; Oddo, S.; Tran, L.X.; LaFerla, F.M. Lithium reduces tau phosphorylation but not Aβ or working memory deficits in a transgenic model with both plaques and tangles. Am. J. Pathol. 2007, 170, 1669–1675. [Google Scholar] [CrossRef]
- Torrisi, S.; Geraci, F.; Tropea, M.; Grasso, M.; Caruso, G.; Fidilio, A.; Musso, N.; Sanfilippo, G.; Tascedda, F.; Palmeri, A. Fluoxetine and vortioxetine reverse depressive-like phenotype and memory deficits induced by Aβ1-42 oligomers in mice: A key role of transforming growth factor-β1. Front. Pharmacol. 2019, 10, 693–707. [Google Scholar] [CrossRef]
- Caraci, F.; Tascedda, F.; Merlo, S.; Benatti, C.; Spampinato, S.F.; Munafò, A.; Leggio, G.M.; Nicoletti, F.; Brunello, N.; Drago, F. Fluoxetine prevents Aβ1-42-induced toxicity via a paracrine signaling mediated by transforming-growth-factor-β1. Front. Pharmacol. 2016, 7, 389. [Google Scholar] [CrossRef] [PubMed]
- Beyazyüz, M.; Albayrak, Y.; Eğilmez, O.B.; Albayrak, N.; Beyazyüz, E. Relationship between SSRIs and metabolic syndrome abnormalities in patients with generalized anxiety disorder: A prospective study. Psychiatry Investig. 2013, 10, 148. [Google Scholar] [CrossRef]
- Tin, G.; Mohamed, T.; Shakeri, A.; Pham, A.T.; Rao, P.P. Interactions of selective serotonin reuptake inhibitors with β-amyloid. ACS Chem. Neurosci. 2018, 10, 226–234. [Google Scholar] [CrossRef] [PubMed]
- Swerdlow, R.H. Mitochondria and mitochondrial cascades in Alzheimer’s disease. J. Alzheimer’s Dis. 2018, 62, 1403–1416. [Google Scholar] [CrossRef]
- Cova, I.; Clerici, F.; Rossi, A.; Cucumo, V.; Ghiretti, R.; Maggiore, L.; Pomati, S.; Galimberti, D.; Scarpini, E.; Mariani, C.; et al. Weight loss predicts progression of mild cognitive impairment to Alzheimer’s disease. PLoS ONE 2016, 11, e0151710. [Google Scholar] [CrossRef] [PubMed]
- Li, J.Q.; Tan, L.; Wang, H.F.; Tan, M.S.; Tan, L.; Xu, W.; Zhao, Q.F.; Wang, J.; Jiang, T.; Yu, J.T. Risk factors for predicting progression from mild cognitive impairment to Alzheimer’s disease: A systematic review and meta-analysis of cohort studies. J. Neurol. Neurosurg. Psychiatry 2016, 87, 476–484. [Google Scholar] [CrossRef]
- Qizilbash, N.; Gregson, J.; Johnson, M.E.; Pearce, N.; Douglas, I.; Wing, K.; Evans, S.J.W.; Pocock, S.J. BMI and risk of dementia in two million people over two decades: A retrospective cohort study. Lancet Diabetes Endocrinol. 2015, 3, 431–436. [Google Scholar] [CrossRef]
- Chen, Y.; Silverstone, T. Lithium and weight gain. Int. Clin. Psychopharmacol. 1990, 5, 217–226. [Google Scholar] [CrossRef] [PubMed]
- Huang, M.; Liang, Y.; Chen, H.; Xu, B.; Chai, C.; Xing, P. The role of fluoxetine in activating Wnt/β-catenin signaling and repressing β-amyloid production in an Alzheimer mouse model. Front. Aging Neurosci. 2018, 10, 164. [Google Scholar] [CrossRef] [PubMed]
- Trapp, S.; Cork, S.C. PPG neurons of the lower brain stem and their role in brain GLP-1 receptor activation. Am. J. Physiol.-Regul. Integr. Comp. Physiol. 2015, 309, R795–R804. [Google Scholar] [CrossRef] [PubMed]
- He, Z.; Gao, Y.; Lieu, L.; Afrin, S.; Cao, J.; Michael, N.J.; Dong, Y.; Sun, J.; Guo, H.; Williams, K.W. Direct and indirect effects of liraglutide on hypothalamic POMC and NPY/AgRP neurons–Implications for energy balance and glucose control. Mol. Metab. 2019, 28, 120–134. [Google Scholar] [CrossRef] [PubMed]
- Gharagozloo, M.; Galleguillos, D.; Jank, L.; Sotirchos, E.S.; Smith, M.D.; Garton, T.; Kumar, S.; Hussein, O.; Potluri, S.; Taylor, M. The Effects of NLY01, a Novel Glucagon-Like Peptide-1 Receptor Agonist, on Cuprizone-Induced Demyelination and Remyelination: Challenges and Future Perspectives. Neurotherapeutics 2023, 20, 1229–1240. [Google Scholar] [CrossRef] [PubMed]
- Reiner, D.J.; Mietlicki-Baase, E.G.; McGrath, L.E.; Zimmer, D.J.; Bence, K.K.; Sousa, G.L.; Konanur, V.R.; Krawczyk, J.; Burk, D.H.; Kanoski, S.E. Astrocytes regulate GLP-1 receptor-mediated effects on energy balance. J. Neurosci. 2016, 36, 3531–3540. [Google Scholar] [CrossRef]
- Cui, Q.N.; Stein, L.M.; Fortin, S.M.; Hayes, M.R. The role of glia in the physiology and pharmacology of glucagon-like peptide-1: Implications for obesity, diabetes, neurodegeneration and glaucoma. Br. J. Pharmacol. 2022, 179, 715–726. [Google Scholar] [CrossRef]
- Nystrom, T.; Gutniak, M.K.; Zhang, Q.; Zhang, F.; Holst, J.J.; Ahrén, B.; Sjoholm, A. Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease. Am. J. Physiol.-Endocrinol. Metab. 2004, 287, E1209–E1215. [Google Scholar] [CrossRef] [PubMed]
- Bailey, J.; Coucha, M.; Bolduc, D.R.; Burnett, F.N.; Barrett, A.C.; Ghaly, M.; Abdelsaid, M. GLP-1 receptor nitration contributes to loss of brain pericyte function in a mouse model of diabetes. Diabetologia 2022, 65, 1541–1554. [Google Scholar] [CrossRef]
- Rhea, E.M.; Babin, A.; Thomas, P.; Omer, M.; Weaver, R.; Hansen, K.; Banks, W.A.; Talbot, K. Brain uptake pharmacokinetics of albiglutide, dulaglutide, tirzepatide, and DA5-CH in the search for new treatments of Alzheimer’s and Parkinson’s diseases. Tissue Barriers 2023, 2292461. [Google Scholar] [CrossRef]
- Cukierman-Yaffe, T.; Gerstein, H.C.; Colhoun, H.M.; Diaz, R.; García-Pérez, L.-E.; Lakshmanan, M.; Bethel, A.; Xavier, D.; Probstfield, J.; Riddle, M.C. Effect of dulaglutide on cognitive impairment in type 2 diabetes: An exploratory analysis of the REWIND trial. Lancet Neurol. 2020, 19, 582–590. [Google Scholar] [CrossRef]
- Zhou, M.; Chen, S.; Peng, P.; Gu, Z.; Yu, J.; Zhao, G.; Deng, Y. Dulaglutide ameliorates STZ induced AD-like impairment of learning and memory ability by modulating hyperphosphorylation of tau and NFs through GSK3β. Biochem. Biophys. Res. Commun. 2019, 511, 154–160. [Google Scholar] [CrossRef]
- Gray, E.; Ginty, M.; Kemp, K.; Scolding, N.; Wilkins, A. The PPAR-γ agonist pioglitazone protects cortical neurons from inflammatory mediators via improvement in peroxisomal function. J. Neuroinflamm. 2012, 9, 63. [Google Scholar] [CrossRef]
- Kanakasabai, S.; Pestereva, E.; Chearwae, W.; Gupta, S.K.; Ansari, S.; Bright, J.J. PPARγ agonists promote oligodendrocyte differentiation of neural stem cells by modulating stemness and differentiation genes. PLoS ONE 2012, 7, e50500. [Google Scholar] [CrossRef]
Elements | Refs. |
---|---|
Aβ deposition ↑ | [20,21] |
Tau deposition ↑ | [22] |
ApoE4ɛ ↑ | [5] |
Autophagy ↓ | [3,4] |
Ca2+ dysregulation ↑ | [5] |
Circadian dysrhythmia ↑ | [6,7] |
Depression ↑ | [8] |
Diabetes ↑ | [9] |
Epigenetics ↑ | [10] |
Inflammation ↑ | [11] |
Hypertension | |
Hyperlipidemia | [25] |
Insulin resistance ↑ | [12] |
Metabolic syndrome ↑ | |
Mitochondrial dysfunction ↑ | [27] |
Neuronal/synaptic dysfunctions ↑ | [14,15,16] |
Nutrient (folate and vitamin D deficiencies) ↑ | |
TGF-β deficiency ↑ | |
Underweight ↑ | [28,29,30] |
Vascular pathologies ↑ | [17] |
Wnt/catenin-β ↓ | [18,19] |
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Fessel, J. Special Issue “Pathophysiology and Treatment of Alzheimer’s Disease”. Int. J. Mol. Sci. 2024, 25, 6015. https://doi.org/10.3390/ijms25116015
Fessel J. Special Issue “Pathophysiology and Treatment of Alzheimer’s Disease”. International Journal of Molecular Sciences. 2024; 25(11):6015. https://doi.org/10.3390/ijms25116015
Chicago/Turabian StyleFessel, Jeffrey. 2024. "Special Issue “Pathophysiology and Treatment of Alzheimer’s Disease”" International Journal of Molecular Sciences 25, no. 11: 6015. https://doi.org/10.3390/ijms25116015