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

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

Find studies

Showing 3,151–3,175 of 10,985 studies · free to read (page 127 of 440) · 27,380 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; 12,859 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.

Divergent roles of ALS-linked proteins FUS/TLS and TDP-43 intersect in processing long pre-mRNAs

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature neuroscience 2012-09-30

FUS/TLS (fused in sarcoma/translocated in liposarcoma) and TDP-43 are integrally involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 1 key finding →

Evidence: low

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

The overlap between vascular disease and Alzheimer's disease--lessons from pathology

✓ Peer-reviewed alzhub usefulness score 56 out of 100. BMC medicine 2014-11-11

Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer's disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline. 5 key findings →

Evidence: low

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

Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2013-10-16

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap. 2 key findings →

Evidence: low

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

C9orf72 is required for proper macrophage and microglial function in mice

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Science (New York, N.Y.) 2016-03-01

Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 2 key findings →

Evidence: low

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

Cytoplasmic TDP-43 De-mixing Independent of Stress Granules Drives Inhibition of Nuclear Import, Loss of Nuclear TDP-43, and Cell Death

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neuron 2019-03-07

While cytoplasmic aggregation of TDP-43 is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia, how aggregates form and what drives its nuclear clearance have not been determined. 1 key finding →

Evidence: low

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

Abnormality of gait as a predictor of non-Alzheimer's dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The New England journal of medicine 2002-11-01

The presence of neurologic gait abnormalities in elderly persons without dementia at base line is a significant predictor of the risk of development of dementia, especially non-Alzheimer's dementia. 3 key findings →

Participants: 422 Evidence: low

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

Caspase activation precedes and leads to tangles

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature 2010-03-31

Studies of post-mortem tissue have shown that the location of fibrillar tau deposits, called neurofibrillary tangles (NFT), matches closely with regions of massive neuronal death, severe cytological abnormalities, and markers of caspase activation and apoptosis, leading to the idea that tangles cause neurodegeneration in Alzheimer's disease and tau-related frontotemporal dementia. 2 key findings →

Evidence: low

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

Controversies and priorities in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2013-03-01

Two decades after the discovery that 20% of familial amyotrophic lateral sclerosis (ALS) cases were linked to mutations in the superoxide dismutase-1 (SOD1) gene, a substantial proportion of the remainder of cases of familial ALS have now been traced to an expansion of the intronic hexanucleotide repeat sequence in C9orf72. 1 key finding →

Evidence: low

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

Different regional patterns of cortical thinning in Alzheimer's disease and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Brain : a journal of neurology 2007-03-12

Alzheimer's disease and frontotemporal dementia (FTD) can be difficult to differentiate clinically because of overlapping symptoms. 5 key findings →

Participants: 22 Evidence: low

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

Interactions of pathological proteins in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2017-04-11

Neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTD), Lewy body disease (LBD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) have in common that protein aggregates represent pathological hallmark lesions. 1 key finding →

Evidence: low

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

Alzheimer's disease versus dementia with Lewy bodies: cerebral metabolic distinction with autopsy confirmation

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Annals of neurology 2001-09-01

Seeking antemortem markers to distinguish Dementia with Lewy bodies (DLB) and Alzheimer's disease (AD), we examined brain glucose metabolism of DLB and AD. 5 key findings →

Participants: 53 Evidence: low

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

TDP-43 Pathology in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Molecular neurodegeneration 2021-12-20

Transactive response DNA binding protein of 43 kDa (TDP-43) is an intranuclear protein encoded by the TARDBP gene that is involved in RNA splicing, trafficking, stabilization, and thus, the regulation of gene expression. 3 key findings →

Evidence: low

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

TREM2 deficiency impairs chemotaxis and microglial responses to neuronal injury

✓ Peer-reviewed alzhub usefulness score 56 out of 100. EMBO reports 2017-05-08

Sequence variations in the triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to an increased risk for neurodegenerative disorders such as Alzheimer's disease and frontotemporal lobar degeneration. 2 key findings →

Evidence: low

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

A review on neuroimaging-based classification studies and associated feature extraction methods for Alzheimer's disease and its prodromal stages

✓ Peer-reviewed alzhub usefulness score 56 out of 100. NeuroImage 2017-04-13

Neuroimaging has made it possible to measure pathological brain changes associated with Alzheimer's disease (AD) in vivo. 2 key findings →

Evidence: low

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

Incidence of dementia and cognitive impairment, not dementia in the United States

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Annals of neurology 2011-03-18

The incidence of CIND is greater than the incidence of dementia, and those with CIND are at high risk of progressing to dementia, making CIND a potentially valuable target for treatments aimed at slowing cognitive decline. 1 key finding →

Participants: 456 Evidence: low

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

Altered Gut Microbial Metabolites in Amnestic Mild Cognitive Impairment and Alzheimer's Disease: Signals in Host-Microbe Interplay

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nutrients 2021-01-14

Intimate metabolic host-microbiome crosstalk regulates immune, metabolic, and neuronal response in health and disease, yet remains untapped for biomarkers or intervention for disease. 2 key findings →

Participants: 77 Evidence: moderate

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

Subjective cognitive concerns and neuropsychiatric predictors of progression to the early clinical stages of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2014-02-26

From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI. 1 key finding →

Design: longitudinal study Evidence: moderate

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

Metabolic abnormalities associated with mild cognitive impairment in Parkinson disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 2008-03-26

The quantification of these alterations with (18)F-fluorodeoxyglucose PET may allow for the objective assessment of the progression and treatment of this disease manifestation. 2 key findings →

Participants: 18 Evidence: moderate

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

↑ 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.

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