30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
For 11 AD cases and four normal elderly controls, post mortem volumes of the hippocampal subdivisions were calculated by using magnetic resonance imaging and histological sections. 1 key finding →
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
The patterns of subfield atrophy in AD and MCI were consistent with patterns of neuronal cell loss/reduced synaptic density described by histopathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From clinical studies it is known that recurrent depressive episodes associate with a reduced hippocampal volume. 3 key findings →
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
Animal studies on the effects of chronic variable stress during the peripubertal-juvenile period on hippocampal structure and function are lacking. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In chronic alcoholism, the reduction of hippocampal volume is proportional to the reduction of the brain volume. 4 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
Patients with Parkinson's disease (PD) may have hippocampal atrophy compared with controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Smaller hippocampal volume is not a necessary risk factor for developing PTSD and does not occur within 6 months of expressing the disorder. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
MRI studies using the manual tracing method have shown a smaller-than-normal hippocampal volume in patients with posttraumatic stress disorder (PTSD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Theories of the pathophysiology of schizophrenia have implicated the hippocampus, but controversy remains regarding hippocampal abnormalities in patients with schizophrenia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hippocampus is known to support recollection memory, but the relation between its structure and recollection in healthy adults has not been established. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontal lobe abnormalities may occur as a result of PTSD in children or, alternatively, be a risk factor for the development of the syndrome in this age group. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Acute stress suppresses new cell birth in the hippocampus in several species. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structural deformity of the hippocampus is characteristic of individuals with very mild and mild forms of dementia of the Alzheimer type (DAT). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite the ongoing fundamental controversy about the physiological function of sleep, there is general consensus that sleep benefits neuronal plasticity, which ultimately supports brain function and cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results replicate previous findings of reduced hippocampal volume in PTSD but also suggest independent, generalized, white matter atrophy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data provide further evidence of structural brain abnormalities in geriatric depression, particularly in patients with a longer course of illness. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prior work has demonstrated that the memory dysfunction of Alzheimer's disease (AD) is accompanied by marked cortical pathology in medial temporal lobe (MTL) gray matter. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Studies have suggested that teens with alcohol use disorder (AUD) can demonstrate memory deficits, but the underlying neuroanatomical substrates are unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic stress in non-human animals decreases the volume of the hippocampus, a brain region that supports learning and memory and that regulates neuroendocrine activity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epilepsy is a common outcome of traumatic brain injury (TBI), but the mechanisms of posttraumatic epileptogenesis are poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Posttraumatic stress disorder (PTSD) is associated with long-term changes in neurobiology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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.
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.
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