Previously published community- or population-based studies of brain aging and dementia with autopsy were restricted to a single sex, a single ethnic group, Roman Catholic clergy, or focused pathological assessments. 2 key findings →
Design: longitudinal study
Participants: 221
Evidence: moderate
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The pathologic indices of Alzheimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older persons with and without dementia, but the extent to which they account for late life cognitive decline remains unknown. 4 key findings →
Design: longitudinal study
Participants: 856
Evidence: moderate
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This longitudinal quantitative magnetic resonance imaging study of 24 patients with mild temporal lobe epilepsy shows an ipsilateral hippocampal volume decrease of 9% (range, -30 to +0.5%; p = 0.002, paired t test) over a period of 3.5 +/- 0.7 years. 2 key findings →
Design: longitudinal study
Participants: 24
Evidence: moderate
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We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. 4 key findings →
Design: cohort study
Participants: 1,666
Evidence: moderate
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Olfaction and color vision identify early-stage synuclein-mediated neurodegenerative diseases. 3 key findings →
Design: prospective cohort
Participants: 64
Evidence: moderate
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PM2.5 exposure may contribute to WM loss in older women. 2 key findings →
Evidence: low
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NFTs in the substantia nigra are associated with gait impairment in older persons with and without dementia. 4 key findings →
Design: longitudinal study
Participants: 86
Evidence: moderate
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Layer II of the entorhinal cortex contains the cells of origin for the perforant path, plays a critical role in memory processing, and consistently degenerates in end-stage Alzheimer's disease. 5 key findings →
Design: longitudinal study
Participants: 29
Evidence: moderate
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Stable isotope labeling of CNS proteins can be utilized to assess the effects of drugs on the production and clearance rates of proteins targeted as potential disease-modifying treatments for Alzheimer's disease and other CNS disorders. 2 key findings →
Evidence: low
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The use of an amyloid clock enabled visualization and analysis of biomarker changes as a function of estimated years from symptom onset in sporadic AD. 1 key finding →
Design: cross-sectional
Participants: 118
Evidence: moderate
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In DIAD, solanezumab was not associated with ARIA. 5 key findings →
Design: cross-sectional
Participants: 52
Evidence: moderate
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Cerebrovascular disease is a significant and potentially preventable cause of dementia in the Baltimore Longitudinal Study of Aging. 5 key findings →
Design: longitudinal study
Participants: 179
Evidence: moderate
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This approach, describing the 14 years preceding dementia, provides a clear illustration of the particularly long and progressive prodromal phase of AD, and shows the successive emergence of cognitive deficits, depressive symptoms, and functional impairment during this phase. 2 key findings →
Design: case-control study
Participants: 350
Evidence: moderate
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Older, healthy women with decreased circadian activity rhythm amplitude and robustness, and delayed rhythms have increased odds of developing dementia and MCI. 3 key findings →
Design: cross-sectional
Evidence: moderate
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Our findings indicate that tau accumulates even in amyloid-negative healthy OA and this process can be measured with in vivo tau-PET. 5 key findings →
Design: longitudinal study
Evidence: moderate
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Among the evaluated parameters, the only significant predictor of conversion to AD was non-Cp copper (hazard ratio = 1.23, 95% confidence interval = 1.03-1.47, p = 0.022); for each additional micromole per liter unit (μmol/l) of non-Cp copper, the hazard increased by ~20%. 2 key findings →
Design: meta-analysis
Participants: 42
Evidence: high
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Vascular health had quantifiably greater impact on neurodegeneration in AD regions than on amyloid deposition. 3 key findings →
Design: longitudinal study
Participants: 430
Evidence: moderate
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CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging. 1 key finding →
Design: longitudinal study
Participants: 164
Evidence: moderate
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Plasma Abeta42/Abeta40 ratio has potential as a prescreener to identify Alzheimer pathological changes in cognitively normal individuals with SCD. 2 key findings →
Participants: 248
Evidence: moderate
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Atherosclerosis has been implicated in the development of dementia and its major subtypes, Alzheimer's disease and vascular dementia. 4 key findings →
Design: cohort study
Participants: 6,647
Evidence: moderate
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MarkVCID2 enrolled 1883 individuals age 73.4 ± 7.5 years, 65.0% female, 24.2% Hispanic, and 27.1% non-Hispanic Black. 5 key findings →
Design: longitudinal study
Participants: 1,883
Evidence: moderate
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Atherosclerosis of the intracranial arteries is an independent and important risk factor for dementia, suggesting potentially reversible pathways unrelated to Alzheimer pathology and stroke through which vascular changes may influence dementia risk. 2 key findings →
Design: longitudinal study
Participants: 200
Evidence: moderate
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Immunization against amyloid-beta has been suggested as a possible preventive or therapeutic treatment for Alzheimer's disease. 1 key finding →
Design: longitudinal study
Participants: 365
Evidence: moderate
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A case-control study was performed to determine the possible roles of various environmental factors, prior illnesses, drug use, and personal habits in the development of Alzheimer's disease. 4 key findings →
Design: case-control study
Participants: 40
Evidence: moderate
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Aβ deposition increases slowly from cognitive normality to moderate severity DAT. 5 key findings →
Participants: 206
Evidence: low
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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
- Randomized / 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
- Multicenter 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 31,780 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.