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We have detailed the degenerative changes that occur in several neuronal populations, including the cholinergic neurons in the nucleus basalis of Meynert, the histaminergic neurons in the tuberomammillary nucleus, the serotonergic neurons in the raphe nuclei, and the noradrenergic neurons in the locus coeruleus. Furthermore, we discuss the potential role of iron accumulation in the brains of subjects with AD in the disease progression which served as a basis for the idea that iron chelation in the brain may mitigate oxidative stress and decelerate disease development. We also draw attention to possible role of sympathetic system and, more specifically, noradrenergic neurons of the superior cervical ganglion in triggering of the disease. We also explore the alternative possibility of compensatory protective changes that may occur in these neurons to support cholinergic function in the forebrain of subjects with AD.<\/jats:p>","DOI":"10.3233\/jad-240620","type":"journal-article","created":{"date-parts":[[2024,9,10]],"date-time":"2024-09-10T10:42:32Z","timestamp":1725964952000},"page":"1043-1061","source":"Crossref","is-referenced-by-count":2,"title":["Alzheimer\u2019s Disease: An Attempt of Total Recall"],"prefix":"10.1177","volume":"101","author":[{"given":"Alexey P.","family":"Bolshakov","sequence":"first","affiliation":[{"name":"Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantin","family":"Gerasimov","sequence":"additional","affiliation":[{"name":"Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia"},{"name":"Russian National Research Medical University, Moscow, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yulia V.","family":"Dobryakova","sequence":"additional","affiliation":[{"name":"Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-240620_ref1","doi-asserted-by":"crossref","first-page":"2716","DOI":"10.1038\/s41380-023-02076-1","article-title":"Step by step: Towards a better understanding of the genetic architecture of Alzheimer\u2019s disease","volume":"28","author":"Lambert","year":"2023","journal-title":"Mol Psychiatry"},{"key":"10.3233\/JAD-240620_ref2","doi-asserted-by":"crossref","first-page":"4260","DOI":"10.1016\/j.cell.2023.08.021","article-title":"Alzheimer\u2019s disease: From immunotherapy to immunoprevention","volume":"186","author":"Jucker","year":"2023","journal-title":"Cell"},{"key":"10.3233\/JAD-240620_ref3","doi-asserted-by":"crossref","first-page":"5481","DOI":"10.1038\/s41380-021-01249-0","article-title":"The amyloid-\u03b2 pathway in Alzheimer\u2019s disease","volume":"26","author":"Hampel","year":"2021","journal-title":"Mol Psychiatry"},{"key":"10.3233\/JAD-240620_ref4","first-page":"1","article-title":"A\u03b2 plaques","volume":"1","author":"Walker","year":"2020","journal-title":"Free Neuropathol"},{"key":"10.3233\/JAD-240620_ref5","doi-asserted-by":"crossref","first-page":"2197","DOI":"10.1038\/s41380-023-02113-z","article-title":"Does modulation of tau hyperphosphorylation represent a reasonable therapeutic strategy for Alzheimer\u2019s disease? 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