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Research

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

Find studies

Showing 9,976–10,000 of 27,146 studies marked Peer-reviewed (page 400 of 1086) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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.

Distinct behavioural profiles in frontotemporal dementia and semantic dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of neurology, neurosurgery, and psychiatry 2001-03-01

The findings confirm predictions regarding behavioural differences in frontotemporal and semantic dementia and point to differential roles of the frontal and temporal lobes in affect, social functioning, eating, and compulsive behaviour. 2 key findings →

Participants: 41 Evidence: low

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

The spectrum of pathological involvement of the striatonigral and olivopontocerebellar systems in multiple system atrophy: clinicopathological correlations

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Brain : a journal of neurology 2004-10-27

Multiple system atrophy (MSA) has varying clinical (MSA-P versus MSA-C) and pathological [striatonigral degeneration (SND) versus olivopontocerebellar atrophy (OPCA)] phenotypes. 5 key findings →

Evidence: low

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

Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-05-01

Frontotemporal dementia with parkinsonism, chromosome 17 type (FTDP-17) is caused by mutations in the tau gene, and the signature lesions of FTDP-17 are filamentous tau inclusions. 5 key findings →

Evidence: low

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

Frontotemporal dementia and parkinsonism linked to chromosome 17: a consensus conference. Conference Participants

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Annals of neurology 1997-06-01

We held an international consensus conference on frontotemporal dementia, behavioral disturbances, and parkinsonism linked to chromosome 17 to determine whether these are homogeneous or heterogeneous disorders, to agree on terminology, and to develop strategies for further research. 3 key findings →

Evidence: low

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

The role of TDP-43 propagation in neurodegenerative diseases: integrating insights from clinical and experimental studies

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Experimental & molecular medicine 2020-10-13

TAR DNA-binding protein 43 (TDP-43) is a highly conserved nuclear RNA/DNA-binding protein involved in the regulation of RNA processing. 1 key finding →

Evidence: low

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

Pathogenic implications of mutations in the tau gene in pallido-ponto-nigral degeneration and related neurodegenerative disorders linked to chromosome 17

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1998-10-01

Pallido-ponto-nigral degeneration (PPND) is one of the most well characterized familial neurodegenerative disorders linked to chromosome 17q21-22. 5 key findings →

Evidence: low

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

Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of neuropathology and experimental neurology 2008-06-01

Pathologic TAR-DNA-binding protein 43 (TDP-43) is a disease protein in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis. 4 key findings →

Evidence: low

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

Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 Proteinopathies

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of biological chemistry 2009-01-21

The disease protein in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS) was identified recently as the TDP-43 (TAR DNA-binding protein 43), thereby providing a molecular link between these two disorders. 2 key findings →

Evidence: low

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

Astrocyte pathology and the absence of non-cell autonomy in an induced pluripotent stem cell model of TDP-43 proteinopathy

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-02-11

Glial proliferation and activation are associated with disease progression in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia. 2 key findings →

Evidence: low

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

The progression of pathology in longitudinally followed patients with Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2008-01-30

The present study describes the pathological progression of longitudinally followed cases with levodopa-responsive Parkinson's disease who came to autopsy during the Sydney Multicenter Study of Parkinson's disease. 2 key findings →

Evidence: low

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

Neocortical cholinergic neurons in elderly people

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Lancet (London, England) 1977-03-01

Choline acetyltransferase activity (presynaptic cholinergic system) and high affinity binding of cholinergic antagonists (postsynaptic cholinergic system) were measured in brain tissue removed after death from both mentally normal and demented old people. 2 key findings →

Evidence: low

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

Simultaneous measurement of beta-amyloid(1-42), total tau, and phosphorylated tau (Thr181) in cerebrospinal fluid by the xMAP technology

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Clinical chemistry 2004-11-24

The INNO-BIA AlzBio3 selectively and specifically measured Abeta((1-42)), T-TAU, and P-TAU((181P)) in the CSF. 1 key finding →

Evidence: low

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

Predictive markers for AD in a multi-modality framework: an analysis of MCI progression in the ADNI population

✓ Peer-reviewed alzhub usefulness score 51 out of 100. NeuroImage 2010-12-10

Alzheimer's Disease (AD) and other neurodegenerative diseases affect over 20 million people worldwide, and this number is projected to significantly increase in the coming decades. 4 key findings →

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

Prediction of Alzheimer's disease in subjects with mild cognitive impairment from the ADNI cohort using patterns of cortical thinning

✓ Peer-reviewed alzhub usefulness score 51 out of 100. NeuroImage 2012-10-02

Predicting Alzheimer's disease (AD) in individuals with some symptoms of cognitive decline may have great influence on treatment choice and disease progression. 4 key findings →

Evidence: low

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

Subjective memory complaints and awareness of memory functioning in mild cognitive impairment: a systematic review

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Dementia and geriatric cognitive disorders 2009-08-13

Given the increased risk of progression to dementia for those identified as having MCI, the role of awareness should be explored further with due consideration given to the conceptualization of awareness and the methodology employed. 4 key findings →

Evidence: low

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

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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 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