{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T20:04:36Z","timestamp":1790712276936,"version":"4.1.0"},"reference-count":363,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"American Macular Degeneration Foundation (AMDF), Ocugen Inc."}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Bioengineering"],"abstract":"<jats:p>Alzheimer\u2019s Disease (AD) is a complex neurodegenerative disease resulting in progressive loss of memory, language and motor abilities caused by cortical and hippocampal degeneration. This review captures the landscape of understanding of AD pathology, diagnostics, and current therapies. Two major mechanisms direct AD pathology: (1) accumulation of amyloid \u03b2 (A\u03b2) plaque and (2) tau-derived neurofibrillary tangles (NFT). The most common variants in the A\u03b2 pathway in APP, PSEN1, and PSEN2 are largely responsible for early-onset AD (EOAD), while MAPT, APOE, TREM2 and ABCA7 have a modifying effect on late-onset AD (LOAD). More recent studies implicate chaperone proteins and A\u03b2 degrading proteins in AD. Several tests, such as cognitive function, brain imaging, and cerebral spinal fluid (CSF) and blood tests, are used for AD diagnosis. Additionally, several biomarkers seem to have a unique AD specific combination of expression and could potentially be used in improved, less invasive diagnostics. In addition to genetic perturbations, environmental influences, such as altered gut microbiome signatures, affect AD. Effective AD treatments have been challenging to develop. Currently, there are several FDA approved drugs (cholinesterase inhibitors, A\u00df-targeting antibodies and an NMDA antagonist) that could mitigate AD rate of decline and symptoms of distress.<\/jats:p>","DOI":"10.3390\/bioengineering11010045","type":"journal-article","created":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T13:02:58Z","timestamp":1704114178000},"page":"45","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Alzheimer\u2019s Disease: Models and Molecular Mechanisms Informing Disease and Treatments"],"prefix":"10.3390","volume":"11","author":[{"given":"Kaden L.","family":"Nystuen","sequence":"first","affiliation":[{"name":"Department of Chemical Engineering, University of Massachusetts Amherst, Amherst, MA 01003, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shannon M.","family":"McNamee","sequence":"additional","affiliation":[{"name":"Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica","family":"Akula","sequence":"additional","affiliation":[{"name":"Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina M.","family":"Holton","sequence":"additional","affiliation":[{"name":"Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA"},{"name":"Harvard Stem Cell Institute, Cambridge, MA 02138, USA"},{"name":"Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3731-142X","authenticated-orcid":false,"given":"Margaret M.","family":"DeAngelis","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14203, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4424-9583","authenticated-orcid":false,"given":"Neena B.","family":"Haider","sequence":"additional","affiliation":[{"name":"Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA"},{"name":"Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,1,1]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Wu, Y.-T., Clare, L., Hindle, J.V., Nelis, S.M., Martyr, A., and Matthews, F.E. 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