{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T13:54:26Z","timestamp":1771854866289,"version":"3.50.1"},"reference-count":80,"publisher":"MDPI AG","issue":"13","license":[{"start":{"date-parts":[[2019,7,4]],"date-time":"2019-07-04T00:00:00Z","timestamp":1562198400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>The main risk of Alzheimer\u2019s disease (AD) and Parkinson\u2019s disease (PD), the two most common neurodegenerative pathologies, is aging. In contrast to sporadic cases, whose symptoms appear at &gt;60 years of age, familial PD or familial AD affects younger individuals. Finding early biological markers of these diseases as well as efficacious treatments for both symptom relief and delaying disease progression are of paramount relevance. Familial early-onset PD\/AD are due to genetic factors, sometimes a single mutation in a given gene. Both diseases have neuronal loss and abnormal accumulations of specific proteins in common, but in different brain regions. Despite shared features, the mechanisms underlying the pathophysiological processes are not known. This review aims at finding, among the genetic-associated cases of PD and AD, common trends that could be of interest to discover reliable biomarkers and efficacious therapies, especially those aimed at affording neuroprotection, i.e., the prevention of neuronal death.<\/jats:p>","DOI":"10.3390\/ijms20133297","type":"journal-article","created":{"date-parts":[[2019,7,4]],"date-time":"2019-07-04T11:13:18Z","timestamp":1562238798000},"page":"3297","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Lessons on Differential Neuronal-Death-Vulnerability from Familial Cases of Parkinson\u2019s and Alzheimer\u2019s Diseases"],"prefix":"10.3390","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2549-4919","authenticated-orcid":false,"given":"Rafael","family":"Franco","sequence":"first","affiliation":[{"name":"Chemistry School, University of Barcelona, 08028 Barcelona, Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red Enfermedades Neurodegenerativas (CiberNed), Instituto de Salud Carlos III, 28031 Madrid, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gemma","family":"Navarro","sequence":"additional","affiliation":[{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red Enfermedades Neurodegenerativas (CiberNed), Instituto de Salud Carlos III, 28031 Madrid, Spain"},{"name":"Department of Biochemistry and Physiology, Faculty of Pharmacy, University of Barcelona, 02028 Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0572-0926","authenticated-orcid":false,"given":"Eva","family":"Mart\u00ednez-Pinilla","sequence":"additional","affiliation":[{"name":"Departamento de Morfolog\u00eda y Biolog\u00eda Celular, Facultad de Medicina, Universidad de Oviedo, 33006 Oviedo, Spain"},{"name":"Instituto de Neurociencias del Principado de Asturias (INEUROPA), 33003 Oviedo, Asturias, Spain"},{"name":"Instituto de Salud del Principado de Asturias (ISPA), 33011 Oviedo, Asturias, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2019,7,4]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"277","DOI":"10.3233\/JPD-2011-11046","article-title":"Disentangling the relationship between lewy bodies and nigral neuronal loss in Parkinson\u2019s disease","volume":"1","author":"Parkkinen","year":"2011","journal-title":"J. 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