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These processes are often disrupted by neurodegeneration-induced dementias. Alzheimer\u2019s disease (AD) accounts for 50% of cases of dementia. Vascular dementia (VaD), Parkinson\u2019s disease dementia (PDD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD) constitute much of the remaining cases. While vascular lesions are the principal cause of VaD, neurodegenerative processes have been established as etiological agents of many dementia diseases. Chief among such processes is the deposition of pathological protein aggregates in vivo including \u03b2-amyloid deposition in AD, the formation of neurofibrillary tangles in AD and FTD, and the accumulation of Lewy bodies composed of \u03b1-synuclein aggregates in DLB and PDD. The main symptoms of dementia are cognitive decline and memory and learning impairment. Nonetheless, accurate diagnoses of neurodegenerative diseases can be difficult due to overlapping clinical symptoms and the diverse locations of cortical lesions. Still, new neuroimaging and molecular biomarkers have improved clinicians\u2019 diagnostic capabilities in the context of dementia and may lead to the development of more effective treatments. Both genetic and environmental factors may lead to the aggregation of pathological proteins and altered levels of cytokines, such that can trigger the formation of proinflammatory immunological phenotypes. This cascade of pathological changes provides fertile ground for the development of neural plasticity disorders and dementias. Available pharmacotherapy and disease-modifying therapies currently in clinical trials may modulate synaptic plasticity to mitigate the effects neuropathological changes have on cognitive function, memory, and learning. In this article, we review the neural plasticity changes seen in common neurodegenerative diseases from pathophysiological and clinical points of view and highlight potential molecular targets of disease-modifying therapies.<\/jats:p>","DOI":"10.1155\/2021\/8834645","type":"journal-article","created":{"date-parts":[[2021,3,29]],"date-time":"2021-03-29T18:05:13Z","timestamp":1617041113000},"page":"1-20","source":"Crossref","is-referenced-by-count":19,"title":["Molecular Factors Mediating Neural Cell Plasticity Changes in Dementia Brain Diseases"],"prefix":"10.1155","volume":"2021","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2777-261X","authenticated-orcid":true,"given":"Wojciech","family":"Kozubski","sequence":"first","affiliation":[{"name":"Chair and Department of Neurology, Poznan University of Medical Sciences, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6204-0989","authenticated-orcid":true,"given":"Kevin","family":"Ong","sequence":"additional","affiliation":[{"name":"General Medicine Department, Armadale Health Service, Mount Nasura, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7300-6193","authenticated-orcid":true,"given":"Wioletta","family":"Waleszczyk","sequence":"additional","affiliation":[{"name":"Laboratory of Visual Neurobiology, Department of Neurophysiology, Nencki Institute of Experimental Biology, PAS, Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2591-7379","authenticated-orcid":true,"given":"Matthew","family":"Zabel","sequence":"additional","affiliation":[{"name":"College of Medicine, California Northstate University, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8241-0403","authenticated-orcid":true,"given":"Jolanta","family":"Dorszewska","sequence":"additional","affiliation":[{"name":"Laboratory of Neurobiology, Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1007\/s40520-013-0004-2"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1038\/361031a0"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2202-13-103"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1016\/S0940-9602(11)80255-4"},{"key":"5","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2014.03.001"},{"key":"6","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1973.sp010273"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ne.12.030189.000505"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1327"},{"key":"9","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(89)90026-X"},{"key":"10","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2010.3711"},{"key":"11","doi-asserted-by":"publisher","DOI":"10.1016\/j.arr.2004.05.002"},{"key":"12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M108757200"},{"key":"13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M301938200"},{"key":"14","doi-asserted-by":"publisher","DOI":"10.1016\/j.exger.2010.09.008"},{"key":"15","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.21040"},{"key":"16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205289200"},{"key":"17","doi-asserted-by":"publisher","DOI":"10.3390\/nu11010176"},{"key":"18","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4547(19991001)58:1<10::AID-JNR3>3.0.CO;2-2"},{"key":"19","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresrev.2007.03.011"},{"key":"20","doi-asserted-by":"publisher","DOI":"10.1097\/00005072-199906000-00008"},{"key":"21","doi-asserted-by":"publisher","DOI":"10.1002\/1873-3468.12972"},{"key":"22","doi-asserted-by":"publisher","DOI":"10.1503\/cmaj.070797"},{"key":"23","doi-asserted-by":"crossref","first-page":"1534","DOI":"10.1016\/B978-1-4377-0434-1.00091-8","article-title":"Dementias","volume-title":"Bradley\u2019s Neurology in Clinical Practice","author":"L. 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