Alzheimer's disease
Open accessAbstract
Alzheimer's disease, the commonest cause of dementia, is a growing global health concern with huge implications for individuals and society. In this review, current understanding of the epidemiology, genetics, pathology and pathogenesis of Alzheimer's disease is outlined, before its clinical presentation and current treatment strategies are discussed. Finally, the review discusses how our enhanced understanding of Alzheimer pathogenesis, including the recognition of a protracted preclinical phase, is informing new therapeutic strategies with the aim of moving from treatment to prevention.
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Patients with primary progressive aphasias presenting as agrammatic, semantic or logopenic variants most commonly have frontotemporal lobar degeneration, but hippocampal sparing AD can also present in this manner.
“Patients with primary progressive aphasias presenting as agrammatic, semantic or logopenic variants most commonly have frontotemporal lobar degeneration, but hippocampal sparing AD can also present in this manner [7, 102].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [7]
The vast majority of AD occurs on an apparently sporadic basis (SAD).
“The vast majority of AD occurs on an apparently sporadic basis (sporadic AD or SAD) [54].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [54]
Colombia has the largest and most homogeneous family group known to have an early-onset (~35 years of age) form of FAD caused by the autosomal dominant and fully penetrant E280A mutation in PSEN1.
“Interestingly, Colombia has the largest and most homogeneous family group known to have an early‐onset (~35 years of age) form of FAD [54, 59] caused by the autosomal dominant and fully penetrant E280A mutation in PSEN1 [60, 61], which generally produces a more aggressive course of pathology than SAD [55, 56].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [54]
Aβ42 is more cytotoxic than Aβ40.
“Aβ42 is more cytotoxic than Aβ40 (Lane et al., 2018)”
From Distinct anterograde trafficking pathways of BACE1 and amyloid precursor protein from the TGN and the regulation of amyloid-β production (2020) · cites this paper as Lane et al., 2018
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“This number is predicted to increase to 152 million by 2050 as the population ages [32].”
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AbuAlrob, M. A., Itbaisha, A., Abujwaid, Y. K., Abulehia, A., Hussein, A., & Mesraoua, B. (2025) · Journal of Alzheimer's Disease Reports · doi:10.1177/25424823251388650 · Cited by 10 · see citing works
Xie, M., Wang, T., Feng, J., Ma, D., Feng, L., & Hao, Y. (2025) · Current Neuropharmacology · doi:10.2174/1570159x23666250225091729 · Cited by 7 · see citing works
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Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk
Cohen, C. E., Fernandez, S., Yaman, U., Ehyaei, A. R., Kodosaki, E., Askarova, A., Porter, T., O’Brien, E., Study, A. I. B. A. L., Initiative, A. D. N., et al. (2026) · Alzheimer's Research & Therapy · doi:10.1186/s13195-026-02036-1 · Cited by 1 · see citing works
Self-citation
- Authors
- Lane, C. A., Hardy, J., & Schott, J. M.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- Corresponding author
- Schott, J. M.
- Venue
- European Journal of Neurology
- Publisher
- Wiley
- Published
- 2017-10-19
- Volume
- 25
- Issue
- 1
- Pages
- 59-70
- ISSN
- 1351-5101 (ISSN-L)
- 1468-1331
- OpenAlex
- W4235875658
- Cited by
- 2,616
- References
- 25
- Citations by year
- 2026: 231 · 2025: 343 · 2024: 385 · 2023: 419 · 2022: 424 · 2021: 323 · 2020: 326 · 2019: 127 · 2018: 35 · 2017: 1 · 2012: 1
- FWCI
- 16.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- European Journal of Neurology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wolfson Foundation
- Engineering and Physical Sciences Research Council (EP/J020990/1)
- Medical Research Council (MR/L023784/1)
- Alzheimer’s Research UK (ARUK‐Network 2012‐6‐ICE, ARUK‐PG2017‐1946)
- Brain Research Trust (UCC14191)
- Horizon 2020 (666992)
- Topics
- Health Sciences › Medicine › Physiology › 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, dementia, pathology, pathogenesis, clinical features, treatment options, preclinical stage, prevention
- MeSH terms
- Alzheimer Disease, Brain, Humans
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