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Research

28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,476–1,500 of 7,821 studies · tagged Brain Biology (page 60 of 313) · 28,980 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; 14,457 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.

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

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

Optical Coherence Tomography in Alzheimer's Disease and Other Neurodegenerative Diseases

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Frontiers in neurology 2017-12-19

Over the past decade, a surge of evidence has documented various pathological processes in the retina of patients suffering from mild cognitive impairment, Alzheimer's disease (AD), Parkinson's disease (PD), and other neurodegenerative diseases. 1 key finding →

Design: cross-sectional Evidence: low

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

Amyloid-beta overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2008-12-02

Mitochondrial dysfunction is a prominent feature of Alzheimer disease but the underlying mechanism is unclear. 4 key findings →

Evidence: low

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

Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-07-24

Neural stem cell (NSC) transplantation represents an unexplored approach for treating neurodegenerative disorders associated with cognitive decline such as Alzheimer disease (AD). 4 key findings →

Evidence: low

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

A transgenic Alzheimer rat with plaques, tau pathology, behavioral impairment, oligomeric aβ, and frank neuronal loss

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2013-04-01

Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss (Selkoe, 2001). 4 key findings →

Evidence: low

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

Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature neuroscience 2005-08-28

In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with neurodegeneration and accumulation of amyloid precursor protein (APP) products. 3 key findings →

Evidence: low

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

The Trem2 R47H Alzheimer's risk variant impairs splicing and reduces Trem2 mRNA and protein in mice but not in humans

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Molecular neurodegeneration 2018-09-06

The R47H variant of the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) significantly increases the risk for late onset Alzheimer's disease. 4 key findings →

Evidence: low

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

Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Human molecular genetics 2020-11-01

Genome-wide association studies have reported that, amongst other microglial genes, variants in TREM2 can profoundly increase the incidence of developing Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

TREM2 receptor protects against complement-mediated synaptic loss by binding to complement C1q during neurodegeneration

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Immunity 2023-07-12

Triggering receptor expressed on myeloid cells 2 (TREM2) is strongly linked to Alzheimer's disease (AD) risk, but its functions are not fully understood. 4 key findings →

Evidence: low

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

Viral gene transfer of APPsα rescues synaptic failure in an Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2015-11-04

Alzheimer's disease (AD) is characterized by synaptic failure, dendritic and axonal atrophy, neuronal death and progressive loss of cognitive functions. 4 key findings →

Evidence: low

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

Phospholipids of APOE lipoproteins activate microglia in an isoform-specific manner in preclinical models of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature communications 2021-06-07

APOE and Trem2 are major genetic risk factors for Alzheimer's disease (AD), but how they affect microglia response to Aβ remains unclear. 4 key findings →

Evidence: low

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

Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism

✓ Peer-reviewed alzhub usefulness score 51 out of 100. EMBO molecular medicine 2019-06-01

Microglia adopt numerous fates with homeostatic microglia (HM) and a microglial neurodegenerative phenotype (MGnD) representing two opposite ends. 4 key findings →

Evidence: low

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

From across this tag

10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ Change the filters

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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.

1,038 records (3.6% of the library) are not peer-reviewed — 966 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