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Find studies

Showing 1–25 of 47 studies by Blennow K of type cohort or longitudinal study (page 1 of 2) · 30,180 in the whole library · How the 0–100 score works

Download bibliography of these 47 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

The NfL level was increased at baseline in patients with mild cognitive impairment and AD dementia (mean levels: cognitive unimpairment, 32.1 ng/L; mild cognitive impairment, 37.9 ng/L; and AD dementia, 45.9 ng/L; P Conclusions and relevance The findings suggest that plasma NfL can be used as a noninvasive biomarker associated with neurodegeneration in patients with AD and may be useful to monitor effects in trials of disease-modifying drugs. 3 key findings →

Design: cohort study Participants: 1,583 Evidence: moderate

Plasma p-tau 217 and the NfL/p-tau 217 ratio are promising non-invasive biomarkers for differentiating AD from FTLD, suggesting their use as a potential alternative to traditional diagnostic methods. 2 key findings →

Design: cohort study Participants: 374 Evidence: moderate

Plasma pTau217 is effective for predicting A/T biomarker profile and cognitive decline, though further study is needed to better explain its association with Aβ and tau PET staging. 3 key findings →

Design: longitudinal study Participants: 2,919 Evidence: moderate

Estimating the time course of biomarker changes in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 76 out of 100. Brain : a journal of neurology 2026-06-01

Recent advancements in biomarkers have transformed Alzheimer's disease (AD) diagnosis from being purely symptom-based to include biological criteria. 1 key finding →

Design: longitudinal study Participants: 1,448 Evidence: moderate

Exclusion criteria included any significant neurologic disorder other than suspected AD; presence of infection, infarction, or multiple lacunes as detected by magnetic resonance imaging; and any significant systemic condition that could lead to difficulty complying with the protocol. 3 key findings →

Design: cohort study Participants: 1,113 Evidence: moderate

CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 73 out of 100. Neurology 2018-07-27

Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →

Design: longitudinal study Participants: 508 Evidence: moderate

Detailed comparison of amyloid PET and CSF biomarkers for identifying early Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 72 out of 100. Neurology 2015-09-09

The best CSF measures for identifying MCI-AD were Aβ42/total tau (t-tau) and Aβ42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94). 3 key findings →

Design: longitudinal study Participants: 122 Evidence: moderate

We evaluated the performance of CSF biomarkers for predicting risk of clinical decline and conversion to dementia in non-demented patients with cognitive symptoms. 4 key findings →

Design: longitudinal study Participants: 619 Evidence: moderate

Plasma biomarker profiles in autosomal dominant Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Brain : a journal of neurology 2023-03-01

Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. 4 key findings →

Design: longitudinal study Participants: 164 Evidence: moderate

Our results encourage an independent validation cohort study to confirm the indication that the plasma Aβ 1-40 /Aβ 1-42 ratio, assessed via Simoa, may improve future standard of care and clinical trial design. 2 key findings →

Design: cohort study Participants: 276 Evidence: moderate

Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively. 3 key findings →

Design: longitudinal study Evidence: moderate

In a community-based cohort of 70-year olds, P-NfL was associated with both prevalent and incident CKD, while CSF and/or imaging measures did not differ by CKD status. 3 key findings →

Design: cohort study Participants: 744 Evidence: moderate

Biomarker pattern of ARIA-E participants in phase 3 randomized clinical trials with bapineuzumab

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Neurology 2018-02-02

Baseline biomarkers largely do not predict risk for developing ARIA-E. ARIA-E was associated with significant longitudinal changes in several biomarkers, with larger reductions in amyloid PET and CSF p-tau and t-tau concentrations, and paradoxically greater hippocampal volume reduction and ventricular enlargement, suggesting that ARIA-E in bapineuzumab-treated cases may be related to increased Aβ efflux from the brain and affecting downstream pathogenic processes. 4 key findings →

Design: longitudinal study Participants: 1,512 Evidence: moderate

Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →

Design: longitudinal study Participants: 95 Evidence: moderate

Plasma Aβ42/Aβ40${{\rm A}\beta }_{42}/{{\rm A}\beta }_{40}$ may begin declining decades prior to brain amyloid accumulation, whereas p-tau ratios, GFAP, and NfL increase closer in time. 1 key finding →

Design: longitudinal study Participants: 199 Evidence: moderate

Cerebrospinal fluid tau, neurogranin, and neurofilament light in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. EMBO molecular medicine 2016-10-04

Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →

Design: longitudinal study Participants: 93 Evidence: moderate

We found low intra-individual variability, robust to various factors, appropriate to capture individual changes in AD BBMs, while moderate inter-individual variability may give rise to caution in diagnostic contexts. 2 key findings →

Design: longitudinal study Participants: 27 Evidence: moderate

Increased CSF neurogranin concentration is specific to Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Neurology 2016-01-29

An optimized immunoassay was used to analyze CSF Ng in a retrospective cohort of 331 participants with different neurodegenerative diseases, including healthy controls (n = 19), biomarker-proven Alzheimer disease (AD) (n = 100), genetic AD (n = 2), behavioral variant frontotemporal dementia (n = 20), speech variant frontotemporal dementia (n = 21), Lewy body dementia (n = 13), Parkinson disease (n = 31), progressive supranuclear palsy (n = 46), multiple system atrophy (n = 29), as well as a heterogeneous group with non-neurodegenerative cognitive impairment (n = 50). 1 key finding →

Design: retrospective cohort Participants: 19 Evidence: moderate

The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →

Design: cohort study Participants: 1,593 Evidence: moderate

Blood-Based Biomarkers and Risk of Onset of Mild Cognitive Impairment Over the Short and Long Term

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurology 2024-12-26

This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →

Design: longitudinal study Participants: 271 Evidence: moderate

Choroid plexus (ChP) is emerging as a key brain structure in the pathophysiology of neurodegenerative disorders. 4 key findings →

Design: longitudinal study Participants: 135 Evidence: moderate

Identifying a clinical distinction between the invariably lethal prion disease Creutzfeldt-Jakob disease (CJD) and nonprion rapidly progressive dementias is important and sometimes difficult; thus, reliable tools for diagnosis are in great demand. 4 key findings →

Design: cohort study Participants: 30 Evidence: moderate

Cerebrospinal Fluid Patterns and the Risk of Future Dementia in Early, Incident Parkinson Disease

✓ Peer-reviewed alzhub usefulness score 64 out of 100. JAMA neurology 2015-10-01

Among the 128 study participants, the 104 patients with early PD had a different CSF pattern compared with the 13 patients with progressive supranuclear palsy (baseline area under the receiver operating characteristic curve, 0.87; P < .0001) and the 30 control participants (baseline area under the receiver operating characteristic curve, 0.69; P = .0021). 2 key findings →

Design: cohort study Participants: 104 Evidence: moderate

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 30,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,037 records (3.4% of the library) are not peer-reviewed — 964 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

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