The blood-brain barrier (BBB) represents the interface between the brain and other body tissues. 1 key finding →
Evidence: low
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.
Systemic inflammatory events often precipitate acute cognitive dysfunction in elderly and demented populations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that synaptic dysfunction is a key pathophysiological hallmark in neurodegenerative disorders, including Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
A number of studies indicate that prolonged, major depression is associated with a selective loss of hippocampal volume that persists long after the depression has resolved. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent intriguing reports have shown an association between major depression and selective and persistent loss of hippocampal volume, prompting considerable speculation as to its underlying causes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Smaller hippocampal volume is reported in major depressive disorder (MDD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation and adiposity might relate to cognitive decline via influences on brain morphology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A dysregulated hypothalamic-pituitary-adrenal axis (HPA) has been implicated in major depressive disorder and most commonly used animal models of depression have been shown to elevate circulating levels of plasma corticosterone. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic restraint stress (CRS) induces the remodeling (i.e., retraction and simplification) of the apical dendrites of hippocampal CA3 pyramidal neurons in rats, suggesting that intrahippocampal connectivity can be affected by a prolonged stressful challenge. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Schizophrenia is characterized by reduced hippocampal volume, decreased dendritic spine density, altered neuroplasticity signaling pathways, and cognitive deficits associated with impaired hippocampal function. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We examined the effects of voluntary (16 weeks of wheel running) and forced (16 weeks of treadmill running) exercise on memory-related behavior, hippocampal volume, thioflavine-stained plaque number, and soluble Abeta levels in brain tissue in the Tg2576 mouse model of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hippocampus is crucial for normal brain function, especially for the encoding and retrieval of multimodal sensory information. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impairments in mood and cognitive function are the key brain abnormalities observed in Gulf war illness (GWI), a chronic multisymptom health problem afflicting ∼25% of veterans who served in the Persian Gulf War-1. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucocorticoids (GCs) are hormones secreted by the adrenal glands as an endocrine response to stress. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reduction of cerebral blood flow is an important risk factor for dementia states and other brain dysfunctions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ts65Dn, a well-characterized animal model for Down syndrome, has three copies of the distal end of mouse chromosome 16 and therefore has segmental trisomy for orthologs for nearly half of the genes located on human chromosome 21. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropathologic and neuroradiologic studies have reported hippocampal abnormalities in schizophrenics. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Application of magnetic resonance imaging (MRI) techniques reveals that human brain aging varies across cortical regions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High alcohol consumption for long periods of time causes significant hippocampal neurodegeneration in rodents. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age has a powerful effect on enhanced susceptibility to neurodegenerative diseases, including susceptibility to stroke and cognitive impairment (CI) even in optimally healthy individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Proof that blood-brain barrier failure is key to these conditions could provide a target for new treatments to reduce the effects of vascular disease on the brain and prevent cognitive decline and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tobacco smoke consists of thousands of compounds including nicotine. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Each year, 10 million people worldwide survive the neurologic injury associated with a stroke. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Low-to-moderate red wine consumption appeared to reduce age-related neurological disorders including macular degeneration, stroke, and cognitive deficits with or without dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glutamate is an essential neurotransmitter regulating brain functions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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.
- Molecular genetics of Alzheimer's disease and the amyloid beta peptide precursor gene
- Dynamic changes in plasma biomarkers of Alzheimer's disease in patients treated with lecanemab: a longitudinal cohort study
- Brain-wide Cerebrospinal Fluid Recirculation Collapse in Alzheimer’s Disease
- Preventive and Therapeutic Strategies in Alzheimer's Disease: Focus on Oxidative Stress, Redox Metals, and Ferroptosis
- Limbic-predominant age-related TDP-43 encephalopathy in the oldest old: a population-based study
- Upregulation of select rab GTPases in cholinergic basal forebrain neurons in mild cognitive impairment and Alzheimer's disease
- Microbiome-generated amyloid and potential impact on amyloidogenesis in Alzheimer's disease (AD)
- Apolipoprotein E controls cerebrovascular integrity via cyclophilin A
- Choroid plexus free‐water correlates with glymphatic function in Alzheimer's disease
- Microglia emerge as central players in brain disease
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 →