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57/100

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Mild cognitive impairment

Topic: Risk, prevention and care in population studies

Insulin resistance and type 2 diabetes are associated with cognitive decline and increased risk for Alzheimer's disease (AD). Relatively few studies have assessed the impact of metabolic dysfunction on conversion to AD in mild cognitive impairment (MCI), and it is unclear whether glycemic status is associated with clinically relevant measures of cognitive decline and brain structure in MCI. This study used the Alzheimer's Disease Neuroimaging Initiative database to examine the relationship of baseline glycemia with conversion to AD and longitudinal clinical, cognitive, and imaging measures of decline. Subjects with MCI (n = 264) with baseline and 2-year Clinical Dementia Rating data available were classified according to American Diabetes Association criteria for fasting glucose at baseline. The groups were normoglycemic (fasting glucose, <100 mg/dL; n = 167) or impaired glycemia (fasting glucose, ≥ 100 mg/dL, n = 97). The impaired glycemia group included individuals with fasting glucose that either reached the American Diabetes Association cut point for impaired fasting glucose or individuals with diagnosed diabetes. Two-year change in Clinical Dementia Rating-Sum of Boxes, cognitive performance testing (global cognition), brain volume (whole-brain and hippocampal volume), fluorodeoxyglucose-positron emission tomography, and conversion to AD were assessed. Subjects with normoglycemia at baseline had less functional (Clinical Dementia Rating-Sum of Boxes) and global cognitive decline over 2 years than subjects with impaired glycemia. Subjects with normoglycemia also lost less whole-brain volume and exhibited lower conversion from MCI to AD. There was no difference in hippocampal volume change or fluorodeoxyglucose-positron emission tomography between groups. These results suggest that baseline glycemia is related to cognitive decline and progression to AD.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Morris, J. K., Vidoni, E. D., Honea, R. A., Burns, J. M., & Alzheimer's Disease Neuroimaging Initiative. (2014). Impaired glycemia increases disease progression in mild cognitive impairment. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2013.09.033

Vancouver

Morris JK, Vidoni ED, Honea RA, Burns JM, Alzheimer's Disease Neuroimaging Initiative. Impaired glycemia increases disease progression in mild cognitive impairment. Neurobiology of aging. 2014. doi:10.1016/j.neurobiolaging.2013.09.033. PMID: 24411018.

BibTeX

@article{morris2014-24411018,
  author  = {Morris, J. K. and Vidoni, E. D. and Honea, R. A. and Burns, J. M. and {Alzheimer's Disease Neuroimaging Initiative}},
  title   = {{Impaired glycemia increases disease progression in mild cognitive impairment}},
  journal = {Neurobiology of aging},
  year    = {2014},
  doi     = {10.1016/j.neurobiolaging.2013.09.033},
  pmid    = {24411018},
  url     = {https://doi.org/10.1016/j.neurobiolaging.2013.09.033}
}

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Key findings

Insulin resistance and type 2 diabetes are associated with cognitive decline and increased risk for Alzheimer's disease (AD).
Relatively few studies have assessed the impact of metabolic dysfunction on conversion to AD in mild cognitive impairment (MCI), and it is unclear whether glycemic status is associated with clinically relevant measures of cognitive decline and brain structure in MCI.
These results suggest that baseline glycemia is related to cognitive decline and progression to AD.

Why it matters

Among 264 people with mild cognitive impairment, those with impaired glycemia at baseline showed greater cognitive decline and progression to Alzheimer's disease over two years than those with normal glucose. This is an observational study and does not show that treating impaired glycemia prevents or treats Alzheimer's disease.

Study details

Study designlongitudinal study
Participants264
Evidence strengthModerate

How this study scored 57/100

Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Neurobiology of aging)
Journal's citation record	3 / 4	Neurobiology of Aging: journal h-index 263 (OpenAlex, 2026-10-29)
Study design	7 / 12	A longitudinal study following the same people over time
Strength of evidence	3 / 5	Rated “moderate” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2014 — within 20 year(s) of the newest study here
Sample size	2 / 4	264 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 158 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	11.3 citations a year over 14 year(s) since 2014
Impact for its field and year	4 / 6	Cited 8.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 7 other studies in this library
Still being cited	2 / 4	Cited 20 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Jeffrey Murray Burns: h-index 83 (OpenAlex, whole career)
Institution's track record	0 / 3	University of Kansas Medical Center: institution h-index 578 (OpenAlex)
Multi-centre collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 24411018)
Free to read	0 / 2	Behind a paywall — scores zero
Total	57 / 100	—

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