alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 801–825 of 6,987 studies · tagged Brain Biology (page 33 of 280) · 28,580 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; 14,058 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.

Functional and dynamic polymerization of the ALS-linked protein TDP-43 antagonizes its pathologic aggregation

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature communications 2017-06-29

TDP-43 is a primarily nuclear RNA-binding protein, whose abnormal phosphorylation and cytoplasmic aggregation characterizes affected neurons in patients with amyotrophic lateral sclerosis and frontotemporal dementia. 3 key findings →

Evidence: low

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

Profiles of extracellular miRNA in cerebrospinal fluid and serum from patients with Alzheimer's and Parkinson's diseases correlate with disease status and features of pathology

✓ Peer-reviewed alzhub usefulness score 55 out of 100. PloS one 2014-05-05

The discovery and reliable detection of markers for neurodegenerative diseases have been complicated by the inaccessibility of the diseased tissue--such as the inability to biopsy or test tissue from the central nervous system directly. 2 key findings →

Participants: 69 Evidence: low

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

Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature medicine 2000-08-01

One hallmark of Alzheimer disease is the accumulation of amyloid beta-peptide in the brain and its deposition as plaques. 4 key findings →

Evidence: low

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

TGF-beta1 promotes microglial amyloid-beta clearance and reduces plaque burden in transgenic mice

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature medicine 2001-05-01

Abnormal accumulation of the amyloid-beta peptide (Abeta) in the brain appears crucial to pathogenesis in all forms of Alzheimer disease (AD), but the underlying mechanisms in the sporadic forms of AD remain unknown. 4 key findings →

Evidence: low

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

R47H Variant of TREM2 Associated With Alzheimer Disease in a Large Late-Onset Family: Clinical, Genetic, and Neuropathological Study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA neurology 2015-08-01

The R47H variant in the triggering receptor expressed on myeloid cells 2 gene (TREM2), a modulator of the immune response of microglia, is a strong genetic risk factor for Alzheimer disease (AD) and possibly other neurodegenerative disorders. 4 key findings →

Participants: 751 Evidence: low

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

Clearance of apoptotic neurons without inflammation by microglial triggering receptor expressed on myeloid cells-2

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of experimental medicine 2005-02-01

Elimination of apoptotic neurons without inflammation is crucial for brain tissue homeostasis, but the molecular mechanism has not been firmly established. 4 key findings →

Evidence: low

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

Disease Progression-Dependent Effects of TREM2 Deficiency in a Mouse Model of Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2017-01-01

Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2). 4 key findings →

Evidence: low

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

A TREM2-activating antibody with a blood-brain barrier transport vehicle enhances microglial metabolism in Alzheimer's disease models

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature neuroscience 2023-01-12

Loss-of-function variants of TREM2 are associated with increased risk of Alzheimer's disease (AD), suggesting that activation of this innate immune receptor may be a useful therapeutic strategy. 4 key findings →

Evidence: low

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

Impact of TREM2R47H variant on tau pathology-induced gliosis and neurodegeneration

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of clinical investigation 2020-09-01

Alzheimer's disease (AD) is characterized by plaques containing amyloid-β (Aβ) and neurofibrillary tangles composed of aggregated, hyperphosphorylated tau. 4 key findings →

Evidence: low

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

Activated microglia mitigate Aβ-associated tau seeding and spreading

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of experimental medicine 2021-06-08

In Alzheimer's disease (AD) models, AD risk variants in the microglial-expressed TREM2 gene decrease Aβ plaque-associated microgliosis and increase neuritic dystrophy as well as plaque-associated seeding and spreading of tau aggregates. 4 key findings →

Evidence: low

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

Characterization and clinical use of inflammatory cerebrospinal fluid protein markers in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer's research & therapy 2018-02-26

Neuroinflammation has gained increasing attention as a potential contributing factor in Alzheimer's disease (AD) pathology. 4 key findings →

Participants: 399 Evidence: moderate

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

Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer's continuum when only subtle changes in Aβ pathology are detected

✓ Peer-reviewed alzhub usefulness score 55 out of 100. EMBO molecular medicine 2020-11-10

In Alzheimer's disease (AD), tau phosphorylation in the brain and its subsequent release into cerebrospinal fluid (CSF) and blood is a dynamic process that changes during disease evolution. 4 key findings →

Evidence: low

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

A comparison between tau and amyloid-β cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer's research & therapy 2022-02-09

Cerebrospinal fluid (CSF) tau and beta-amyloid levels in chronic traumatic encephalopathy (CTE), a disease which can be clinically indistinguishable from Alzheimer's disease (AD), are largely unknown. 4 key findings →

Design: cross-sectional Participants: 192 Evidence: low

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

Longitudinal change in CSF Tau and Aβ biomarkers for up to 48 months in ADNI

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2013-06-29

The dynamics of cerebrospinal fluid (CSF) tau and Aβ biomarkers over time in Alzheimer's disease (AD) patients from prodromal pre-symptomatic to severe stages of dementia have not been clearly defined and recent studies, most of which are cross-sectional, present conflicting findings. 4 key findings →

Design: cross-sectional Evidence: moderate

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

Association of CSF Aβ38 Levels With Risk of Alzheimer Disease-Related Decline

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2021-12-22

Experimental studies suggest that the balance between short and long β-amyloid (Aβ) species might modulate the toxic effects of Aβ in Alzheimer disease (AD), but clinical evidence is lacking. 4 key findings →

Participants: 656 Evidence: moderate

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

From across this tag

10 of the 6,970 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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