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Molecular mechanisms of neurodegeneration in Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-beta (Abeta)-containing plaques and neurofibrillary tangles composed of hyperphosphorylated tau. The neurodegenerative process in AD is initially characterized by synaptic damage accompanied by neuronal loss. In addition, recent evidence suggests that alterations in adult neurogenesis in the hippocampus might play a role. Synaptic loss is one of the strongest correlates to the cognitive impairment in patients with AD. Several lines of investigation support the notion that the synaptic pathology and defective neurogenesis in AD are related to progressive accumulation of Abeta oligomers rather than fibrils. Abnormal accumulation of Abeta resulting in the formation of toxic oligomers is the result of an imbalance between the levels of Abeta production, aggregation and clearance. Abeta oligomers might lead to synaptic damage by forming pore-like structures with channel activity; alterations in glutamate receptors; circuitry hyper-excitability; mitochondrial dysfunction; lysosomal failure and alterations in signaling pathways related to synaptic plasticity, neuronal cell and neurogenesis. A number of signaling proteins, including fyn kinase; glycogen synthase kinase-3beta (GSK3beta) and cyclin-dependent kinase-5 (CDK5), are involved in the neurodegenerative progression of AD. Therapies for AD might require the development of anti-aggregation compounds, pro-clearance pathways and blockers of hyperactive signaling pathways.
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“Due to cytosolic calcium overload, p35 splits into p25, which hyperactivates cyclin-dependent kinase-5 (CDK5) and leads to hyper phosphorylation of tau [6].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [6]
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“Moreover, previous findings have suggested a role of Aβ-peptide, generated in mitochondria-associated ER membranes [47], in mediating AD-related excitotoxicity [48] by its physical interaction with NMDAR [49] or by altering glutamate uptake and recycling mechanisms [50].”
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Manchanda, N., Aggarwal, A., Setya, S., & Talegaonkar, S. (2022) · Current Alzheimer Research · doi:10.2174/1567205020666230206124155 · Cited by 20
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“Moreover, the associated signaling cascade is diverse (Seo and Tsai, 2014; Dayer et al., 2015; de Bruin and Kruse, 2015; Ha et al., 2015), including NCAM PSA-immunoreactive neurons in the dentate gyrus, the cyclin-dependent kinase 5, Fyn, Jab1, and mammalian target of rapamycin, SNX14…”
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Fahim, V. F., Wadie, W., Shafik, A. N., & Attallah, M. I. (2018) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2018.10.012 · Cited by 19
The Use of Random Forests to Classify Amyloid Brain PET
Zukotynski, K., Gaudet, V., Kuo, P. H., Adamo, S. M., Goubran, M., Scott, C. J. M., Bocti, C., BORRIE, M. J., Chertkow, H. M., Frayne, R., et al. (2019) · Clinical Nuclear Medicine · doi:10.1097/rlu.0000000000002747 · Cited by 19
The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
Lattanzi, R., Severini, C., Maftei, D., Saso, L., & Badiani, A. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.640441 · Cited by 21
“Aβ Toxicity The presence of extracellular Aβ plaques, tau neurofibrillary tangles and gliosis are associated with the pathogenesis of Alzheimer’s disease (AD) (Akiyama et al., 2000; Crews and Masliah, 2010).”
BackgroundHyperglycosylation is a metabolic driver of Alzheimer’s disease
Hawkinson, T. R., Liu, Z., Ribas, R. A., Medina, T., Nielsen, R. S., Clarke, H. A., Ma, X., Mueller, A. C., Plasencia, A. F., Sheer, A. L., et al. (2026) · Nature Metabolism · doi:10.1038/s42255-026-01538-4 · Cited by 21
Meng, J., Han, L., Zheng, N., Xu, H., Liu, Z., Zhang, X., Luo, H., Can, D., Sun, H., Xu, H., et al. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.596030 · Cited by 19
“Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder characterized by abnormal accumulation and deposition of various amyloid-β (Aβ) peptides derived from amyloid-β precursor protein (APP), formation of neurofibrillary tangles containing hyperphosphorylated tau, synaptic dysfunction, neur…”
BackgroundNiu, T.-T., Yin, H., Xu, B., Yang, T., Li, H., Sun, Y., & Liu, G.-Z. (2022) · Applied Biochemistry and Biotechnology · doi:10.1007/s12010-022-03828-5 · Cited by 20
Berberine: Is it a Promising Agent for Mental Disorders Treatment?
Shayganfard, M. (2022) · Current Molecular Pharmacology · doi:10.2174/1874467215666220509213122 · Cited by 18
Zhang, P., Zhou, Y., Chen, G., Li, J., Wang, B., & Lu, X. (2022) · BMC Musculoskeletal Disorders · doi:10.1186/s12891-022-05580-7 · Cited by 15
“The main pathologies of AD is the aberrant accumulation of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFT) [2, 3].”
BackgroundChiu, P., Yang, F., Chiu, M., Lin, W.-C., Lu, C., & Yang, S. (2022) · Scientific Reports · doi:10.1038/s41598-022-22647-6 · Cited by 20
Printed Biosensors for the Detection of Alzheimer’s Disease Based on Blood Biomarkers
Zeng, Y., Huang, Z., Liu, Y., & Xu, T. (2023) · Journal of Analysis and Testing · doi:10.1007/s41664-023-00277-9 · Cited by 18
“Several theories have been proposed to elucidate the origins of this disorder, including abnormal accumulation of Aβ protein, excessive phosphorylation of tau protein, impairment of cholinergic neurons, oxidative stress, inflammatory responses, and genetic mutations [5–7].”
Manassero, G., Guglielmotto, M., Monteleone, D., Vasciaveo, V., Butenko, O., Tamagno, E., Arancio, O., & Tabaton, M. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170298 · Cited by 17
“As a consequence, tau polymer-izes, since tau-tau binding is stronger than tau-tubulin binding [20].”
Tamano, H., Takiguchi, M., Tanaka, Y., Murakami, T., Adlard, P. A., Bush, A. I., & Takeda, A. (2019) · Molecular Neurobiology · doi:10.1007/s12035-019-01853-w · Cited by 18
“Age-related cognitive decline is believed to be initially due to changes in synaptic function rather than loss of neurons [1], while substantial synaptic and neuronal losses are observed in the early stage of Alzheimer’s disease (AD)when hippocampus-dependent memory loss becomes detectable clinically [2, 3].”
BackgroundTherapeutic Study of Phytochemicals Against Cancer and Alzheimer’s Disease Management
Ahmad, S. S., Waheed, T., Rozeen, S., Mahmood, S., & Kamal, M. A. (2020) · Current Drug Metabolism · doi:10.2174/1389200221666200103092719 · Cited by 18
Cross-Interplay between Osmolytes and mTOR in Alzheimer's Disease Pathogenesis
Mueed, Z., Mehta, D., Rai, P. K., Kamal, M. A., & Poddar, N. K. (2020) · Current Pharmaceutical Design · doi:10.2174/1381612826666200518112355 · Cited by 18
β-Amyloid induces nuclear protease-mediated lamin fragmentation independent of caspase activation
Ramasamy, V. S., Islam, M. R., Haque, M. A., Shin, S. Y., & Park, I. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.02.008 · Cited by 18
Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets
Ahmadi, S., Khaledi, S., Ahmadi, K., & Hassanzadeh, K. (2025) · CNS Neuroscience & Therapeutics · doi:10.1002/cns.70688 · Cited by 20
“These findings indicate that impaired neurogenesis in AD is linked to the dysregulation of CDK5 in neural progenitor cells [23].”
InfluentialWan, L., Liu, D., Xiao, W., Zhang, B., Yan, X., Luo, Z., & Xiao, B. (2021) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-021-01054-x · Cited by 20
Zhu, B., Parsons, T., Stensen, W., Svendsen, J. S. M., Fugelli, A., & Hodge, J. J. L. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.881385 · Cited by 18
“These factors have contributed to the large drug attrition of new drugs that although effective in these rodent models have not translated to any new AD treatments from clinical trials emphasising the need for new molecular models of sporadic AD (McGowan et al., 2006; Crews and Masliah, 2010; Van Dam and De Deyn, 2011…”
BackgroundExploring the effect of gut microbiome on Alzheimer's disease
Pourahmad, R., Saleki, K., Zare, M., Aram, C., Farsani, A. S., Banazadeh, M., & Tafakhori, A. (2024) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2024.101776 · Cited by 20
“This polymerization activates kinases, which can expedite the hyperphosphorylation of tau protein linked with microtubules and the polymerization of tau into insoluble NFTs [20 – 22].”
BackgroundFunctional Amyloidogenesis and Cytotoxicity—Insights into Biology and Pathology
Fowler, D. M., & Kelly, J. W. (2012) · PLoS Biology · doi:10.1371/journal.pbio.1001459 · Cited by 17
“The formation of pores that disrupt membrane structure is also thought to be important in the post-mitotic cell death observed in amyloid disease pathology [23,24]: the hypothesis being that the”
BackgroundBosch, M. N., Gimeno‐Bayón, J., Rodríguez, M. J., Pugliese, M., & Mahy, N. (2013) · Current Alzheimer Research · doi:10.2174/15672050113109990129 · Cited by 17
“correlates more with soluble Aβ brain levels than with Aβ plaque abundance [2,4,5], the amyloid monomers and oligomers are considered to be more toxic [1,6].”
BackgroundAge-Associated Hyper-Methylated Regions in the Human Brain Overlap with Bivalent Chromatin Domains
Watson, C. T., Disanto, G., Sandve, G. K., Breden, F. J., Giovannoni, G., & Ramagopalan, S. V. (2012) · PLoS ONE · doi:10.1371/journal.pone.0043840 · Cited by 17
“Thus, given that one of the primary pathologic features of agerelated neurological disorders such as Alzheimer’s disease and Parkinson’s disease includes the loss of neuronal cell plasticity and cell death [20,21], the relationship between the epigenetic alterations investigated in this study could have involvement in…”
BackgroundNeuroinflammation as a therapeutic target in neurodegenerative diseases
Gordon, R., & Woodruff, T. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-805120-7.00003-8 · Cited by 19
Memorcise and Alzheimer’s disease
Loprinzi, P. D., Frith, E., & Ponce, P. (2018) · The Physician and Sportsmedicine · doi:10.1080/00913847.2018.1445932 · Cited by 17
“Hallmark pathological characteristics of AD include extracellular amyloid beta (Aβ; a main component of amyloid plaques) and intracellular neurofibrillary tangles (NFTs), coupled with neuronal and synaptic loss, vascular amyloidosis, astrocytosis, and microgliosis [29].”
BackgroundSchrauben, M., Dempster, E. L., & Lunnon, K. (2020) · Brain Pathology · doi:10.1111/bpa.12881 · Cited by 17
“The disorder is characterized by the aggregation of amyloid beta (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated tau protein in the cerebral cortex and limbic brain regions, which in turn cause neuronal cell death and thus, cognitive impairment (12).”
BackgroundDo natural antioxidants play a role in Alzheimer's disease?
Lange, K. W., Lange, K. M., Nakamura, Y., & Li, S. (2020) · Journal of Food Bioactives · doi:10.31665/jfb.2020.11233 · Cited by 17
Ucf-101 protects against cerebral oxidative injury and cognitive impairment in septic rat
Hu, Y., Huang, M., Wang, P., Xu, Q., & Zhang, B. (2013) · International Immunopharmacology · doi:10.1016/j.intimp.2013.03.019 · Cited by 17
Lorenzo, R. D., Zecca, C., Chimienti, G., Latronico, T., Liuzzi, G. M., Pesce, V., Dell’Abate, M. T., Borlizzi, F., Giugno, A., Urso, D., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26167792 · Cited by 18
“…neurological disorder involving multiple pathological processes, including neuronal loss, synaptic dysfunction, neuroinflammation, the accumulation of amyloid plaques and neurofibrillary tangles, alterations in lipid and bioenergetics metabolism, oxidative stress, and vascular dysregulation [1].”
The Gut-Brain Axis in Alzheimer’s Disease: Exploring Microbial Influences and Therapeutic Strategies
Mustafa, M. A., Vadia, N., Varma, P., Al‐Shaker, H., Mohanty, B., Dhyani, A., Kaur, I., Chauhan, A. S., & Garg, G. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05474-4 · Cited by 18
“These include the tau hyperphosphorylation theory, the amyloid cascade hypothesis, and mechanisms involving oxidative stress, mitochondrial impairment, and neuroinflammation [32] (Fig.”
Sohn, E., Kim, Y. J., Kim, J., & Jeong, S. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02358-1 · Cited by 16
Neuroprotective Effect of Lutein in Scopolamine-Induced Alzheimer’s Disease in Mice and Zebrafish
Patel, C. A., Patel, P. R., Sarkar, D., Bulsara, J., Soni, A., Isapure, K., & Acharya, S. R. (2021) · Revista Brasileira de Farmacognosia · doi:10.1007/s43450-021-00202-0 · Cited by 16
“Due to this reason, studies on treatment with antioxidants in AD have always been in demand (Crews and Masliah 2010).”
BackgroundRani, N., Sahu, M., Ambasta, R. K., & Kumar, P. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102174 · Cited by 16
Habib, A., Shytle, R. D., Sawmiller, D. R., Koilraj, S., Munna, S. A., Rongo, D., Hou, H., Borlongan, C. V., Currier, G. W., & Tan, J. (2019) · Journal of Neuroscience Research · doi:10.1002/jnr.24438 · Cited by 16
“…consisting of amyloid‐β (Aβ) (Masters et al., 1985) and hyperphosphorylated tau (Grundke‐Iqbal et al., 1986) proteins, respectively, promotes neurodegeneration (Crews & Masliah, 2010) which may be involved in the development of cognitive and neuropsychiatric problems (Lyketsos et al., 2011).”
Background
Metadata
- Authors
- Crews, L., & Masliah, E.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Masliah, E.
- ORCID
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-04-15
- Volume
- 19
- Issue
- R1
- Pages
- R12-R20
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- PMC
- PMC2875049
- OpenAlex
- W2135957529
- Cited by
- 772
- References
- 175
- Citations by year
- 2026: 33 · 2025: 53 · 2024: 56 · 2023: 71 · 2022: 48 · 2021: 76 · 2020: 69 · 2019: 50 · 2018: 47 · 2017: 47 · 2016: 42 · 2015: 34 · 2014: 31 · 2013: 35 · 2012: 40
- FWCI
- 3.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Human Molecular Genetics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AG5131, NS4 4233, AG‐18440, AG10435, AG11385)
- National Institute on Aging (P01AG010435, AG-11385, P50AG005131, AG-5131, AG 18440, AG10435)
- National Institute of Neurological Disorders and Stroke (P01NS044233, NS-44233)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, neurodegeneration, amyloid-beta oligomers, amyloid plaques, tau hyperphosphorylation, neurofibrillary tangles, synaptic loss, adult hippocampal neurogenesis, glutamate receptors, excitotoxicity, mitochondrial dysfunction, lysosomal dysfunction, synaptic plasticity, Fyn, glycogen synthase kinase-3β, cyclin-dependent kinase 5, anti-aggregation therapy, amyloid-beta clearance
- MeSH terms
- Alzheimer Disease, Humans, Amyloid beta-Peptides, Neurogenesis
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