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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 49 studies in Disease mechanisms published 2015 (page 1 of 2) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

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

Other subjects

Authors

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

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

What “Disease mechanisms” covers

Disease mechanisms — Cell- and molecule-level research into what actually goes wrong in Alzheimer's and related diseases.

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.

Cerebrospinal fluid neurogranin: relation to cognition and neurodegeneration in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain : a journal of neurology 2015-09-15

Cerebrospinal fluid neurogranin was increased in patients with Alzheimer's disease dementia (P < 0.001), progressive mild cognitive impairment (P < 0.001) and stable mild cognitive impairment (P < 0.05) compared with controls, and in Alzheimer's disease dementia (P < 0.01) and progressive mild cognitive impairment (P < 0.05) compared with stable mild cognitive impairment. 2 key findings →

Design: longitudinal study Participants: 95 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Souvenaid reduces behavioral deficits and improves social cognition skills in frontotemporal dementia: a proof-of-concept study

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Neuro-degenerative diseases 2015-01-15

Our results provide evidence of the potential of Souvenaid™ therapy for the treatment of behavioral disturbances and social cognition skills in FTD. 2 key findings →

Design: randomized controlled trial Evidence: high

Full summary, score breakdown and related studies → Original source Full text may need a subscription

The role of tau in the pathological process and clinical expression of Huntington's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Brain : a journal of neurology 2015-05-06

Huntington's disease is a neurodegenerative disorder caused by an abnormal CAG repeat expansion within exon 1 of the huntingtin gene HTT. 4 key findings →

Participants: 16 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Recommendations for the use of PET imaging biomarkers in the diagnosis of neurodegenerative conditions associated with dementia: SEMNIM and SEN consensus

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Revista espanola de medicina nuclear e imagen molecular 2015-06-20

The new diagnostic criteria for Alzheimer's disease (AD) acknowledges the interest given to biomarkers to improve the specificity in subjects with dementia and to facilitate an early diagnosis of the pathophysiological process of AD in the prodromal or pre-dementia stage. 5 key findings →

Design: systematic review Evidence: high

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Conserved epigenomic signals in mice and humans reveal immune basis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2015-02-01

Alzheimer's disease (AD) is a severe age-related neurodegenerative disorder characterized by accumulation of amyloid-β plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decline. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

PART is part of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica 2015-01-28

It has been proposed that tau aggregation confined to entorhinal cortex and hippocampus, with no or only minimal Aβ deposition, should be considered as a 'primary age-related tauopathy' (PART) that is not integral to the continuum of sporadic Alzheimer disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2015-04-06

Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). 1 key finding →

Participants: 14 Evidence: low

Full summary, score breakdown and related studies → Original source

A multicenter study of the early detection of synaptic dysfunction in Mild Cognitive Impairment using Magnetoencephalography-derived functional connectivity

✓ Peer-reviewed alzhub usefulness score 41 out of 100. NeuroImage. Clinical 2015-08-01

Synaptic disruption is an early pathological sign of the neurodegeneration of Dementia of the Alzheimer's type (DAT). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

The mTOR Inhibitor Rapamycin Mitigates Perforant Pathway Neurodegeneration and Synapse Loss in a Mouse Model of Early-Stage Alzheimer-Type Tauopathy

✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2015-11-05

The perforant pathway projection from layer II of the entorhinal cortex to the hippocampal dentate gyrus is especially important for long-term memory formation, and is preferentially vulnerable to developing a degenerative tauopathy early in Alzheimer's disease (AD) that may spread over time trans-synaptically. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Cellular Models of Aggregation-dependent Template-directed Proteolysis to Characterize Tau Aggregation Inhibitors for Treatment of Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of biological chemistry 2015-03-10

Alzheimer disease (AD) is a degenerative tauopathy characterized by aggregation of Tau protein through the repeat domain to form intraneuronal paired helical filaments (PHFs). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

In vivo imaging of tau pathology using multi-parametric quantitative MRI

✓ Peer-reviewed alzhub usefulness score 40 out of 100. NeuroImage 2015-02-17

As the number of people diagnosed with Alzheimer's disease (AD) reaches epidemic proportions, there is an urgent need to develop effective treatment strategies to tackle the social and economic costs of this fatal condition. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Degradation of misfolded proteins in neurodegenerative diseases: therapeutic targets and strategies

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Experimental & molecular medicine 2015-03-13

Mammalian cells remove misfolded proteins using various proteolytic systems, including the ubiquitin (Ub)-proteasome system (UPS), chaperone mediated autophagy (CMA) and macroautophagy. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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