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Research

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

Find studies

Showing 9,901–9,925 of 10,985 studies · free to read (page 397 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.

A comparison of cognitive and health assessment tools used in a dementia prevention and risk management program for urban-dwelling older aboriginal Australians (DAMPAA)

✓ Peer-reviewed alzhub usefulness score 36 out of 100. SSM - Mental Health 2025-04-29

There were weak or no correlations between the KICA-Cog and other cognitive assessment tools. 5 key findings →

Participants: 49 Evidence: low

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

Discovering Hidden Links: Harnessing Similarity Network Fusion to Reveal Common Clusters in Healthy Aging, Mild Cognitive Impairment, and Dementia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Alzheimer s & Dementia 2025-12-01

The current study provides evidence that more nuanced, data‐driven approaches can reveal commonalities in the etiology and underlying neurobiology of individuals across traditional categories of CU, MCI, or AD. 5 key findings →

Participants: 515 Evidence: low

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

A single dose of a vectorized mAb targeting TDP-43 potently inhibits the neuropathology in a model of ALS/FTD

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecular Therapy 2025-06-14

Transactive response DNA binding protein-43 (TDP-43)-mediated pathology is a hallmark of devastating neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

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

Chemical and Molecular Strategies in Restoring Autophagic Flux in TDP-43 Proteinopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecules 2026-03-10

The cytoplasmic accumulation of TDP-43 aggregates remains a persistent pathological hallmark of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and limbic-predominant age-related TDP-43 encephalopathy (LATE). 5 key findings →

Evidence: low

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

From Evasion to Collapse: The Kinetic Cascade of TDP-43 and the Failure of Proteostasis

✓ Peer-reviewed alzhub usefulness score 36 out of 100. International Journal of Molecular Sciences 2026-01-23

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases that, despite the availability of symptomatic and modestly beneficial treatments, still lack therapies capable of halting disease progression. 5 key findings →

Evidence: low

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

TDP-43 pathology triggers neuroinflammation and cognitive impairment by inducing microglial necroptosis

✓ Peer-reviewed alzhub usefulness score 36 out of 100. EMBO Molecular Medicine 2026-03-10

Pathological TAR DNA-binding protein-43 (TDP-43) is a defining feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Late-onset dementia with leukoencephalopathy and a COL4A2 gene variant, causal link or fortuitous association: a case report

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cerebral Circulation - Cognition and Behavior 2025-01-01

Cerebral small vessel disease can manifest as vascular dementia, typically associated with vascular risk factors or cerebral amyloid angiopathy, and more rarely associated with hereditary conditions. 5 key findings →

Evidence: low

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

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Acta Neuropathologica Communications 2025-12-02

Dysregulation of the TAR DNA-binding protein 43 (TDP-43), including intraneuronal cytoplasmic mislocalisation and aggregation is a feature of multiple neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal lobar dementia (FTLD), limbic-predominant age-related TDP-43 encephalopathy (LATE) and alzheimer’s disease (AD). 2 key findings →

Evidence: low

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

Delta-opioid receptor ameliorates microglia-induced synapse loss by regulating C1q in Alzheimer disease pathology

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain Behavior and Immunity 2025-10-24

While previous studies have well established δ-opioid receptor (DOR)-mediated neuroprotection against Alzheimer's pathology, the underlying mechanisms remain poorly understood. 2 key findings →

Evidence: low

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

HIV-1 gp120 Interactions with Nicotine Modulate Mitochondrial Network Properties and Amyloid Release in Microglia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurochemical Research 2025-02-24

Human immunodeficiency virus (HIV) infections remain a significant public health burden globally with infected individuals at high risk for cognitive decline and memory loss even on combination antiretroviral therapy. 2 key findings →

Evidence: low

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

Targeting CD38 to alleviate brain endothelial cell dysfunction and cognitive impairment in vascular dementia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Pharmacological Sciences 2025-05-21

Vascular dementia (VaD) is a leading cause of cognitive decline, closely associated with cerebrovascular endothelial cell (CEC) dysfunction, blood-brain barrier (BBB) disruption, and neuroinflammation. 4 key findings →

Evidence: low

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

Cannabidiol and Alzheimer Disease: A Comprehensive Review and In Silico Insights Into Molecular Interactions

✓ Peer-reviewed alzhub usefulness score 36 out of 100. European Journal of Neuroscience 2025-08-01

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a set of multifactorial conditions that progressively impair memory processing and cognitive function. 1 key finding →

Evidence: low

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

Central Insulin-like Growth Factor-1 Treatment Enhances Working and Reference Memory by Reducing Neuroinflammation and Amyloid Beta Deposition in a Rat Model of Sporadic Alzheimer’s Disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Pharmaceuticals 2025-04-04

We found that ICVIGF-1 administration protected working memory demonstrated as (1) reduced latency to reach the platform, and reduced swimming distance in trials 3 (p < 0.05) and 4 (p < 0.01) on days 45 and 90 post-injection and (2) a short-term (up to 45 days post-injection) enhancement of reference memory, manifested by a reduction in swimming distance and latency (p < 0.05). 3 key findings →

Participants: 40 Evidence: low

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

Novel Dual Mechanism GRT-X Agonist Acting on Kv7 Potassium Channel/Translocator Protein Receptor Prevents Motoneuron Degeneration Following Exposure to Mouse and Human Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Astrocyte-Conditioned Media

✓ Peer-reviewed alzhub usefulness score 36 out of 100. ACS Chemical Neuroscience 2025-07-17

High Resolution Image Download MS PowerPoint Slide Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) form a continuous spectrum of aggressive neurodegenerative diseases affecting primarily motoneurons (MNs) and cortical frontotemporal neurons. 5 key findings →

Evidence: low

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

Elucidating molecular pathogenesis and developing targeted therapeutic interventions for cerebrovascular endothelial cell-mediated vascular dementia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Frontiers in Aging Neuroscience 2025-07-16

Vascular dementia (VaD) ranks as the second most prevalent subtype of dementia, surpassed only by Alzheimer's disease (AD). 5 key findings →

Evidence: low

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

Volatile oil of Acori tatarinowii rhizoma: potential candidate drugs for mitigating dementia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Frontiers in Pharmacology 2025-04-23

The volatile oil of ATR mitigates dementia through multiple pathways, including reducing abnormal protein aggregation, promoting neurogenesis, inhibiting neuronal apoptosis, regulating neurotransmitters, improving synaptic function, modulating autophagy, countering cellular stress, reducing neuroinflammation, and alleviating vascular risk factors. 4 key findings →

Evidence: low

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

Direct and indirect role of non-coding RNAs in company with amyloid and tau protein in promoting neuroinflammation in post-ischemic brain neurodegeneration

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Frontiers in Cellular Neuroscience 2025-10-31

Post-ischemic brain neurodegeneration with subsequent neuroinflammation is a major cause of mortality, permanent disability, and the development of Alzheimer’s disease type dementia in the absence of appropriate treatment. 5 key findings →

Evidence: low

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

Xixin Decoction’s novel mechanism for alleviating Alzheimer’s disease cognitive dysfunction by modulating amyloid-β transport across the blood–brain barrier to reduce neuroinflammation

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Frontiers in Pharmacology 2025-01-06

Modern clinical studies have demonstrated its significant therapeutic effects in treating Alzheimer’s disease (AD) without notable adverse reactions. 4 key findings →

Evidence: low

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

Air pollution and Alzheimer disease phenotype deplete esterified proresolving lipid mediator reserves in the brain

✓ Peer-reviewed alzhub usefulness score 36 out of 100. JCI Insight 2025-05-13

BACKGROUNDTraffic-related air pollution (TRAP) is a risk factor for Alzheimer disease (AD), where unresolved brain inflammation has been linked to deficits in the levels of free lipid mediators that enable the resolution of inflammation. 2 key findings →

Evidence: low

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

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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.

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