We systematically reviewed randomized clinical trials of problem-solving therapy (PST) in older adults. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Scores from domains were summed and classified into 3 categories: 4 or less, minimal; 5-12, moderate; and more than 12, significant content. 4 key findings →
Participants: 58 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Medication-free nonelderly depressed outpatients without alcohol dependence or adverse experiences in childhood had normal hippocampal volume. 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Changes in human HFV associated with sustained hypercortisolemia are reversible, at least in part, once cortisol levels decrease. 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
In major depression, decreased hippocampal volume has been attributed to hypercortisolemia, a frequent sign of the disorder, because in animals an excess of corticosteroids has led to dendritic atrophy, astrogliosis and loss of neurons in this brain region. 1 key finding →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
This study provides genetic evidence supporting the potential therapeutic benefits of targeting the three druggable genes for AD treatment, which will be useful for prioritising AD drug development. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing life expectancy has led to an aging population, which has consequently increased the prevalence of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Biomarkers of neurodegeneration and neuronal injury have the potential to improve diagnostic accuracy, disease monitoring, prognosis, and measure treatment efficacy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Better diagnostic tools at initial evaluation may reduce unnecessary delays in access to treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are the resident macrophages of the central nervous system (CNS) acting as the first line of defense in the brain by phagocytosing harmful pathogens and cellular debris. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ability to investigate therapeutic interventions in animal models of neurodegenerative diseases depends on extensive characterization of the model(s) being used. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ferroptosis and neuroinflammation play crucial roles in Alzheimer's disease (AD) pathophysiology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauvid has been approved by the U.S. Food and Drug Administration (FDA) in 2020 for positron emission tomography (PET) imaging of adult patients with cognitive impairments undergoing evaluation for Alzheimer's disease (AD) based on tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hereditary diseases are caused by mutations in genes, and more than 7,000 rare diseases affect over 30 million Americans. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab recently underwent two large phase III clinical trials that were stopped prematurely by the sponsor Biogen. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Immunotherapy against amyloid-beta (Aβ) is a promising option for the treatment of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a devastating age-related neurodegenerative disorder with an alarming increasing prevalence. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab has been approved by the US Food and Drug Administration for treatment of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent form of age-related dementia in the world, and its main pathological features consist of amyloid-β (Aβ) plaque deposits and neurofibrillary tangles formed by hyperphosphorylated tau protein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Two anti-amyloid monoclonal antibodies (MABs)-lecanemab (Leqembi ® ) and aducanumab (Aduhelm ® )-have been approved in the USA for the treatment of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
However, while Aβ may contribute to disease, genetic, clinical, imaging and biochemical data suggest a more complex aetiology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Currently, there is no disease-modifying treatment available for Alzheimer's and Parkinson's disease (AD and PD) and that includes the highly controversial approval of the Aβ-targeting antibody aducanumab for the treatment of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disease in the elderly worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative old age disease that is complex, multifactorial, unalterable, and progressive in nature. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,106 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.
- Amyloid-related imaging abnormalities: manifestations, metrics and mechanisms
- Dynamic changes in plasma biomarkers of Alzheimer's disease in patients treated with lecanemab: a longitudinal cohort study
- The impact of individual Cognitive Stimulation Therapy (iCST) on cognition, quality of life, caregiver health, and family relationships in dementia: A randomised controlled trial
- Semaglutide-mediated protection against Aβ correlated with enhancement of autophagy and inhibition of apotosis
- Changes in Out-of-Pocket Drug Expenditures Among Medicare Beneficiaries With Dementia Under the Inflation Reduction Act: A Simulation Study
- Treatment of cardiovascular risk factors to prevent cognitive decline and dementia: a systematic review
- Plants with traditional uses and activities, relevant to the management of Alzheimer's disease and other cognitive disorders
- A Phase II, Randomized, Double-Blind, Placebo-Controlled Study of Safety, Pharmacokinetics, and Biomarker Results of Subcutaneous Bapineuzumab in Patients with mild to moderate Alzheimer's disease
- Identification of Hasegawa Dementia Scale‐Revised Cutoff Scores Associated With Mini‐Mental State Examination Thresholds for Anti‐Amyloid β Therapies in Patients With Amnesia
- Integrating Multisource Target Evidence with Machine-Learning Potency Prediction for Alzheimer’s Disease Drug Discovery
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 →