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Find studies

Showing 201–225 of 317 studies published 2012 · free to read (page 9 of 13) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of these 317 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.

Neuroinflammation is associated with virtually all major neurodegenerative disorders, including Alzheimer's disease (AD). 4 key findings →

Evidence: moderate

Arch Neurol. 2008;65(7):963-967.) for the Mini-Mental State Examination in detecting cognitive dysfunction in a bilingual sample of highly educated ethnically diverse individuals. 4 key findings →

Participants: 7,093 Evidence: moderate

Accumulation of the amyloid β (Aβ) peptide within the brain is hypothesized to be one of the main causes underlying the pathogenic events that occur in Alzheimer disease (AD). 4 key findings →

Evidence: low

Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neurology 2012-05-02

Of the 296 initially normal subjects, 31 (10%) progressed to a diagnosis of mild cognitive impairment (MCI) or dementia (27 amnestic MCI, 2 nonamnestic MCI, and 2 non-AD dementias) within 1 year. 1 key finding →

Evidence: low

This software program with application of SPM8 plus DARTEL to VBM provides a high performance for AD diagnosis by using MRI. 1 key finding →

Participants: 45 Evidence: low

Physical activity reduces the risk of cognitive impairment, mainly vascular dementia, in older people living independently. 1 key finding →

Participants: 90 Evidence: low

Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neuroinflammation 2012-07-02

Accumulating evidence suggests that neuroinflammation, mediated by the brain's innate immune system, contributes to AD neuropathology and exacerbates the course of the disease. 5 key findings →

Evidence: low

Proline isomer-specific antibodies reveal the early pathogenic tau conformation in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Cell 2012-03-01

cis-trans isomerization of proteins phosphorylated by proline-directed kinases is proposed to control numerous signaling molecules and is implicated in the pathogenesis of Alzheimer's and other diseases. 5 key findings →

Evidence: low

Memory clinic patients were administered the MoCA, MMSE, and a comprehensive formal neuropsychological battery. 4 key findings →

Participants: 36 Evidence: low

The AB Cognitive Screen (ABCS) 135, sensitive in differentiating MCI from dementia, was modified to improve sensitivity and specificity, producing the quick mild cognitive impairment (Qmci) screen. 4 key findings →

Participants: 630 Evidence: low

Increasing evidence suggests a role of atherosclerosis in the pathogenesis of cognitive impairment and dementia. 4 key findings →

Participants: 844 Evidence: low

The Framingham Brain Donation Program: neuropathology along the cognitive continuum

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Current Alzheimer research 2012-07-01

The Framingham Heart Study has enrolled 3 generations of participants, the original cohort (gen 1) enrolled in 1948, the offspring cohort (gen 2) enrolled in 1971 and the third generation enrolled in 2002. 4 key findings →

Participants: 59 Evidence: moderate

Maternal family history is associated with Alzheimer's disease biomarkers

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of Alzheimer's disease : JAD 2012-01-01

A family history of Alzheimer's disease (AD) increases one's risk of developing late-onset AD (LOAD), and a maternal family history of LOAD influences risk more than a paternal family history. 4 key findings →

Design: cross-sectional Participants: 99 Evidence: low

Abnormal deposition and intercellular propagation of α-synuclein plays a central role in the pathogenesis of disorders such as Parkinson's Disease (PD) and dementia with Lewy bodies (DLB). 4 key findings →

Evidence: low

Higher student-teacher ratio was associated with worse cognitive function and greater school year length was associated with better cognitive function. 5 key findings →

Participants: 433 Evidence: low

One of the pathological hallmarks of Alzheimer disease is the accumulation of amyloid plaques in the extracellular space in the brain. 2 key findings →

Evidence: low

Cerebrovascular disease has an important role in cognitive decline and dementia. 5 key findings →

Evidence: low

Investigation of dopaminergic transporter loss in vivo using (123)I-N-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl) nortropane single photon emission computed tomography has been widely used as a diagnostic aid in Lewy body disease. 3 key findings →

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.

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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% of the library) are not peer-reviewed — 962 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 →

Newest studies, as a dated timeline →    Atom feed