Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments
Alzheimer’s 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 me...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-01-01
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| Series: | Bioengineering |
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| Online Access: | https://www.mdpi.com/2306-5354/11/1/45 |
| _version_ | 1797344640972619776 |
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| author | Kaden L. Nystuen Shannon M. McNamee Monica Akula Kristina M. Holton Margaret M. DeAngelis Neena B. Haider |
| author_facet | Kaden L. Nystuen Shannon M. McNamee Monica Akula Kristina M. Holton Margaret M. DeAngelis Neena B. Haider |
| author_sort | Kaden L. Nystuen |
| collection | DOAJ |
| description | Alzheimer’s 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 β (Aβ) plaque and (2) tau-derived neurofibrillary tangles (NFT). The most common variants in the Aβ pathway in <i>APP</i>, <i>PSEN1,</i> and <i>PSEN2</i> are largely responsible for early-onset AD (EOAD), while <i>MAPT</i>, <i>APOE</i>, <i>TREM2</i> and <i>ABCA7</i> have a modifying effect on late-onset AD (LOAD). More recent studies implicate chaperone proteins and Aβ 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, Aß-targeting antibodies and an NMDA antagonist) that could mitigate AD rate of decline and symptoms of distress. |
| first_indexed | 2024-03-08T11:05:40Z |
| format | Article |
| id | doaj.art-bf3971ef913347aeafe2a1c4a2737b76 |
| institution | Directory Open Access Journal |
| issn | 2306-5354 |
| language | English |
| last_indexed | 2024-03-08T11:05:40Z |
| publishDate | 2024-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Bioengineering |
| spelling | doaj.art-bf3971ef913347aeafe2a1c4a2737b762024-01-26T15:06:16ZengMDPI AGBioengineering2306-53542024-01-011114510.3390/bioengineering11010045Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and TreatmentsKaden L. Nystuen0Shannon M. McNamee1Monica Akula2Kristina M. Holton3Margaret M. DeAngelis4Neena B. Haider5Department of Chemical Engineering, University of Massachusetts Amherst, Amherst, MA 01003, USASchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USASchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USADepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USADepartment of Ophthalmology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14203, USASchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USAAlzheimer’s 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 β (Aβ) plaque and (2) tau-derived neurofibrillary tangles (NFT). The most common variants in the Aβ pathway in <i>APP</i>, <i>PSEN1,</i> and <i>PSEN2</i> are largely responsible for early-onset AD (EOAD), while <i>MAPT</i>, <i>APOE</i>, <i>TREM2</i> and <i>ABCA7</i> have a modifying effect on late-onset AD (LOAD). More recent studies implicate chaperone proteins and Aβ 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, Aß-targeting antibodies and an NMDA antagonist) that could mitigate AD rate of decline and symptoms of distress.https://www.mdpi.com/2306-5354/11/1/45Alzheimer’s Diseaseamyloid βTau |
| spellingShingle | Kaden L. Nystuen Shannon M. McNamee Monica Akula Kristina M. Holton Margaret M. DeAngelis Neena B. Haider Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments Bioengineering Alzheimer’s Disease amyloid β Tau |
| title | Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments |
| title_full | Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments |
| title_fullStr | Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments |
| title_full_unstemmed | Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments |
| title_short | Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments |
| title_sort | alzheimer s disease models and molecular mechanisms informing disease and treatments |
| topic | Alzheimer’s Disease amyloid β Tau |
| url | https://www.mdpi.com/2306-5354/11/1/45 |
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