Late-onset Alzheimer Disease
Rabinovici GD.. Continuum (Minneapolis, Minn.), 2019-02-01
Topic: Amyloid, tau and blood-test diagnosis
Purpose of review Alzheimer disease (AD) is the most common cause of late-onset dementia. This article describes the epidemiology, genetic and environmental risk factors, clinical diagnosis, biomarkers, and treatment of late-onset AD, defined by age of onset of 65 years or older. Recent findings An estimated 5.7 million Americans are living with AD dementia, with the number of affected individuals growing rapidly because of an aging population. Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease. The primary genetic risk factor for late-onset AD is the apolipoprotein E (APOE) ε4 allele. AD typically presents with early and prominent episodic memory loss, although this clinical syndrome is neither sensitive nor specific for underlying AD neuropathology. Emerging CSF and imaging biomarkers can now detect the key neuropathologic features of the disease (amyloid plaques, neurofibrillary tangles, and neurodegeneration) in living people, allowing for characterization of patients based on biological measures. A comprehensive treatment plan for AD includes use of symptomatic medications, optimal treatment of comorbid conditions and neuropsychiatric symptoms, counseling about safety and future planning, and referrals to community resources. Summary AD is very common in older neurologic patients. Neurologists should set the standard for the diagnosis and care of patients with AD and should be familiar with emerging biomarkers that have transformed AD research and are primed to enter the clinical arena.
Key findings
- Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease.
Why it matters
This review describes that vascular risk factors, sleep disorders, and traumatic brain injury are associated with increased Alzheimer's disease risk, while increased cognitive and physical activity throughout life reduce risk, and that APOE ε4 is the primary genetic risk factor. It also notes that a comprehensive treatment plan includes symptomatic medications and care for comorbid conditions, and it does not report a cure or prevention.
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Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record and institution's track record, so those were left out: it earned 43 of the 93 points we could judge it on, which is 46 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Continuum (Minneapolis, Minn.)) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 166 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 18.4 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 4 / 6 | Cited 11.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 3 / 4 | Cited 81 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Gil D. Rabinovici: h-index 116 (OpenAlex, whole career) |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30707185) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 43 / 93 | Scored on 18 of 20 parts. We have no data for the rest, so they are left out: 43 of the 93 points we could judge it on is 46 out of 100. |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1212/con.0000000000000700
- PubMed: 30707185
- Original source →
- Free full text: PubMed Central →
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Rabinovici, G. D. (2019). Late-onset Alzheimer Disease. Continuum (Minneapolis, Minn.). https://doi.org/10.1212/con.0000000000000700
Vancouver
Rabinovici GD. Late-onset Alzheimer Disease. Continuum (Minneapolis, Minn.). 2019. doi:10.1212/con.0000000000000700. PMID: 30707185.
BibTeX
@article{rabinovici2019-30707185,
author = {Rabinovici, G. D.},
title = {{Late-onset Alzheimer Disease}},
journal = {Continuum (Minneapolis, Minn.)},
year = {2019},
doi = {10.1212/con.0000000000000700},
pmid = {30707185},
url = {https://doi.org/10.1212/con.0000000000000700}
}
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