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A number of clinical findings have reported peripheral disorders among AD patients. Amyloid beta (A\u03b2) is a toxic physiological aggregate that serves as\u00a0a triggering factor for hepatic and cardiac disorders related to neurotoxicity. As a drawback of A\u03b2 excessive accumulation in the brain, part of A\u03b2 is believed to readily cross the blood\u2013brain barrier (BBB) into the peripheral circulation resulting in serious inflammatory and toxic cascades acting as a direct bridge to cardiac and hepatic pathophysiology. The main aim is to find out whether neuroinflammation-related AD may result in cardiac and liver dysfunctions. Potential therapeutic interventions are also suggested to alleviate AD\u2019s cardiac and hepatic defects. Male rats were divided into: control group I, lipopolysaccharide (LPS)-neuroinflammatory-induced group II, LPS-neuroinflammatory-induced group treated with sodium hydrogen sulphide donor (NaHS) (group III), and LPS-neuroinflammatory-induced group treated with mesenchymal stem cells (MSCs) (group IV). Behavior and histopathological studies were conducted in addition to the estimation of different biological biomarkers. It was revealed that the increased toxic A\u03b2 level in blood resulted in cardiac and hepatic malfunctions as a drawback of exaggerated inflammatory cascades. The administration of NaHS and MSCs proved their efficiency in combating neuroinflammatory drawbacks by hindering cardiac and hepatic dysfunctions. The consistent direct association of decreased heart and liver functions with increased A\u03b2 levels highlights the direct involvement of AD in other organ complications. Thereby, these findings will open new avenues for combating neuroinflammatory-related AD and long-term asymptomatic toxicity.<\/jats:p><jats:p><jats:bold>Graphic abstract<\/jats:bold><\/jats:p>","DOI":"10.1007\/s10787-023-01202-3","type":"journal-article","created":{"date-parts":[[2023,4,5]],"date-time":"2023-04-05T10:40:05Z","timestamp":1680691205000},"page":"1257-1277","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Hepatic and cardiac implications of increased toxic amyloid-beta serum level in lipopolysaccharide-induced neuroinflammation in rats: new insights into alleviating therapeutic interventions"],"prefix":"10.1007","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1991-2945","authenticated-orcid":false,"given":"Mai M.","family":"Anwar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abeer A.","family":"Mabrouk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2023,4,5]]},"reference":[{"key":"1202_CR1","doi-asserted-by":"publisher","first-page":"893","DOI":"10.1016\/j.clinbiochem.2007.04.017","volume":"40","author":"MT Abdel Aziz","year":"2007","unstructured":"Abdel Aziz MT, Atta HM, Mahfouz S, Fouad HH, Roshdy NK, Ahmed HH, Rashed LA, Sabry D, Hassouna AA, Hasan NM (2007) Therapeutic potential of bone marrow-derived mesenchymal stem cells on experimental liver fibrosis. 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