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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 151–175 of 303 studies published 2014 · free to read (page 7 of 13) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 303 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.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 13,658 studies have no institution on record and are not counted here.

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.

Association of hypometabolism and amyloid levels in aging, normal subjects

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 2014-05-02

Hypometabolism in PiB-positive, cognitively normal subjects in a population-based cohort occurs in AD-signature cortical regions and to a lesser extent in other cortical regions. 4 key findings →

Design: cross-sectional Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Automated quantification of 18F-flutemetamol PET activity for categorizing scans as negative or positive for brain amyloid: concordance with visual image reads

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2014-08-21

The derived threshold was used to categorize the 172 scans in the test cohort as negative or positive, and results were compared with categorization using visual assessment. 4 key findings →

Participants: 68 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Epidemiology and outcomes in community-acquired versus hospital-acquired AKI

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Clinical journal of the American Society of Nephrology : CJASN 2014-03-27

The incidence of CA-AKI among all hospital admissions was 4.3% compared with an incidence of 2.1% of HA-AKI, giving an overall AKI incidence of 6.4%. 2 key findings →

Participants: 15,976 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neuron 2014-12-01

Expanded GGGGCC (G4C2) nucleotide repeats within the C9ORF72 gene are the most common genetic mutation associated with both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Human molecular genetics 2014-02-18

Intronic expansion of a hexanucleotide GGGGCC repeat in the chromosome 9 open reading frame 72 (C9ORF72) gene is the major cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Journal of neurochemistry 2014-04-19

The β-site APP cleaving enzymes 1 and 2 (BACE1 and BACE2) were initially identified as transmembrane aspartyl proteases cleaving the amyloid precursor protein (APP). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Frontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Acta neuropathologica 2014-12-31

Frontotemporal lobar degeneration (FTLD) comprises two main classes of neurodegenerative diseases characterized by neuronal/glial proteinaceous inclusions (i.e., proteinopathies) including tauopathies (i.e., FTLD-Tau) and TDP-43 proteinopathies (i.e., FTLD-TDP) while other very rare forms of FTLD are known such as FTLD with FUS pathology (FTLD-FUS). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Mild to moderate Alzheimer dementia with insufficient neuropathological changes

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Annals of neurology 2014-04-08

Recently, ~16% of participants in an anti-Aβ passive immunotherapy trial for mild-to-moderate Alzheimer disease (AD) had a negative baseline amyloid positron emission tomography (PET) scan. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Asymmetry and heterogeneity of Alzheimer's and frontotemporal pathology in primary progressive aphasia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Brain : a journal of neurology 2014-02-25

The most common and distinctive feature for all pathologies associated with primary progressive aphasia was the asymmetric prominence of atrophy, neuronal loss, and disease-specific proteinopathy in the language-dominant (mostly left) hemisphere. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Management of neuropsychiatric symptoms of dementia in clinical settings: recommendations from a multidisciplinary expert panel

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of the American Geriatrics Society 2014-03-17

Noncognitive neuropsychiatric symptoms (NPS) of dementia (aggression, agitation, depression, anxiety, delusions, hallucinations, apathy, disinhibition) affect individuals with dementia nearly universally across dementia stages and etiologies. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Physiological and functional consequences of caregiving for relatives with dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. International psychogeriatrics 2014-02-10

There is accumulating evidence that chronic dementia caregiver stress increases their vulnerability to disease and diminishes their ability to provide optimal care. 2 key findings →

Participants: 4,145 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Subjective cognitive complaints contribute to misdiagnosis of mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of the International Neuropsychological Society : JINS 2014-08-26

Subjective cognitive complaints are a criterion for the diagnosis of mild cognitive impairment (MCI), despite their uncertain relationship to objective memory performance in MCI. 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Upregulation of TREM2 ameliorates neuropathology and rescues spatial cognitive impairment in a transgenic mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2014-07-22

Triggering receptor expressed on myeloid cells 2 (TREM2) gene is a recently identified susceptibility gene for Alzheimer's disease (AD), as its low-frequency variants increase the risk of this disease with an odds ratio similar to that of an APOE ɛ4 allele. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Homozygous TREM2 mutation in a family with atypical frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurobiology of aging 2014-04-18

TREM2 mutations were first identified in Nasu-Hakola disease, a rare autosomal recessive disease characterized by recurrent fractures because of bone cysts and presenile dementia. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Differential roles of the ubiquitin proteasome system and autophagy in the clearance of soluble and aggregated TDP-43 species

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of cell science 2014-01-14

TAR DNA-binding protein (TDP-43, also known as TARDBP) is the major pathological protein in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Adipokines: a link between obesity and dementia?

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Lancet. Neurology 2014-09-01

Being overweight or obese, as measured with body-mass index or central adiposity (waist circumference), and the trajectory of body-mass index over the life course have been associated with brain atrophy, white matter changes, disturbances of blood-brain barrier integrity, and risk of all-cause late-onset dementia and Alzheimer's disease. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Plasma biosignature and brain pathology related to persistent cognitive impairment in late-life depression

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Molecular psychiatry 2014-08-05

Cognitive impairment is highly prevalent among individuals with late-life depression (LLD) and tends to persist even after successful treatment. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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