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.

Find studies

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.

Genetic susceptibility to Lewy body disease and the distribution of Lewy pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-24

Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant. 4 key findings →

Design: meta-analysis Participants: 1,362 Evidence: high

Structured Metabolic Genetic Axes Reveal Distinct Lipid and Ketone-Body Programs in Alzheimer’s and Parkinson’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-19

Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association. 1 key finding →

Evidence: low

APOEε4 attenuates early TREM2-mediated microglial responses and influences disease trajectories in dementia with Lewy bodies

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-31

Dementia with Lewy bodies (DLB) is characterized by marked biological heterogeneity, only partly explained by the frequent presence of Alzheimer’s disease (AD) copathology. 4 key findings →

Design: longitudinal study Participants: 129 Evidence: moderate

Residualized WMH T1w/T2w-FLAIR ratio captures lesion-specific microstructural variation missed by volumetric measures, consistent with vascular-gliotic injury in VD and coexisting amyloid-linked demyelination in AD. 4 key findings →

Design: cross-sectional Participants: 71 Evidence: moderate

Normative transcriptomic clues to thalamic developmental vulnerability in C9orf7 2-FTLD

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-13

This study investigated volumetric MRI differences of the thalamic nuclei in asymptomatic young adult C9orf72 expansion carriers compared to non-carriers, and examined spatial associations with normative thalamic transcriptomics from 8 weeks post-conception through middle age. 3 key findings →

Participants: 72 Evidence: low

Information-Theoretic Geometry HCFIM features for data-limited EEG screening of Alzheimer’s disease and Frontotemporal Dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-13

Resting-state EEG is a scalable modality for neurophysiological screening, but conventional spectral descriptors capture only part of the signal organization altered in neurodegenerative disease. 1 key finding →

Evidence: high

The Somnogenesis System: A Proposed Biological System for Psychiatry

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-08

For more than 150 years, since the idea that mental illness is rooted in the brain first emerged in the mid-1800s, psychiatry has searched for a reliable biological system to anchor its understanding of mental illness. 5 key findings →

Evidence: low

Conformation-based detection of tau seeds with a novel VHH

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2025-12-08

In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →

Evidence: low

Glucagon-Like Peptide-1 Receptor Agonists and Risk of Parkinsonian Disorders in Patients with Obesity

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-02

Among adults with obesity or overweight with a weight related condition, there was no difference in the risk of PD or Parkinsonian disorders between GLP-1 RA users and non-users. 4 key findings →

Design: cohort study Participants: 11,683 Evidence: moderate

Neurodegenerative diseases are a major threat to older adults and represent a growing global health burden as the elderly population continues to expand. 1 key finding →

Evidence: low

Treatment of obstructive sleep apnea may contribute to long-term stabilisation of memory in Alzheimer's and vascular dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-10

Controlling for baseline differences, treatment of OSA improved delayed recall and may reduce the slope of memory decline in Alzheimer’s disease and vascular dementia. 3 key findings →

Design: cohort study Participants: 86 Evidence: moderate

Age-Related Speech-in-Noise Hearing Loss in Parkinson’s Disease and APOE E4 Carriers

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-06-09

Age-related hearing loss is a leading modifiable risk factor for dementia and is increasingly recognized as a non-motor feature of Parkinson’s disease (PD). 4 key findings →

Design: longitudinal study Evidence: moderate

Oligodendrocyte stress response as a driver of vascular dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13

Vascular dementia (VaD) is a prevalent and devastating neurocognitive disorder characterized by profound white matter damage, yet the precise cellular mechanisms linking cerebrovascular stress to demyelination remain poorly understood. 1 key finding →

Evidence: low

In this bvFTD cohort, structural volumes of key frontotemporal and perisylvian regions did not predict behavioral or language impairments after correction for multiple comparisons. 3 key findings →

Design: longitudinal study Participants: 87 Evidence: moderate

The ability to decode others’ emotions from multisensory cues is central to social functioning. 3 key findings →

Design: systematic review Participants: 1,511 Evidence: high

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Overlapping Phenotypes and Associations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-14

Traumatic brain injury (TBI), chronic traumatic encephalopathy (CTE), and Alzheimer's disease (AD) share several neuropathophysiological mechanisms, including axonal injury, neuroinflammation, and abnormal protein aggregation, which may contribute to overlapping clinical manifestations. 1 key finding →

Evidence: low

The study evaluated 1,457 PD patients (1,050 primary; 407 secondary) alongside 2,100 matched non-PD controls. 5 key findings →

Design: cross-sectional Evidence: low

Panel-Gene Transcriptomic Associations and Published-Variant Architecture in Parkinson Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-22

Parkinson disease (PD) was examined in four primary adult-brain GEO cohorts (GSE49036, GSE20141, GSE8397, GSE7621) using a frozen 468-gene redox, metal, xenobiotic, and barrier panel. 1 key finding →

Design: meta-analysis Evidence: high

Upper cervical spinal cord morphometric charts: from population references to individualized clinical assessment

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-12

The upper cervical spinal cord is essential for motor, sensory and autonomic function, yet its normative morphometric trajectories and disease-related deviations remain unclear. 2 key findings →

Participants: 2,394 Evidence: low

Spermine inhibits ferroptosis in vascular dementia rats by intervening Nrf2/SLC7A11/GPX4 expression in chondriosome

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-09

Spermine exerts neuroprotective effects in VaD by inhibiting TRPM2-mediated oxidative stress and activating the Nrf2/SLC7A11/GPX4 pathway, thereby suppressing ferroptosis. 3 key findings →

Evidence: low

From across this tag

10 of the 2,823 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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    Where this research is being discussed: events