Cited by 185Alzheimer's disease research and treatmentsAmino Acid Enzymes and MetabolismDementia and Cognitive Impairment Research

Amino acid catabolism in Alzheimer’s disease brain: Friend or foe?

Open access
Griffin, Jeddidiah W. D., Bradshaw, Patrick C.·2017·Oxidative Medicine and Cellular Longevity

Abstract

There is a dire need to discover new targets for Alzheimer's disease (AD) drug development. Decreased neuronal glucose metabolism that occurs in AD brain could play a central role in disease progression. Little is known about the compensatory neuronal changes that occur to attempt to maintain energy homeostasis. In this review using the PubMed literature database, we summarize evidence that amino acid oxidation can temporarily compensate for the decreased glucose metabolism, but eventually altered amino acid and amino acid catabolite levels likely lead to toxicities contributing to AD progression. Because amino acids are involved in so many cellular metabolic and signaling pathways, the effects of altered amino acid metabolism in AD brain are far-reaching. Possible pathological results from changes in the levels of several important amino acids are discussed. Urea cycle function may be induced in endothelial cells of AD patient brains, possibly to remove excess ammonia produced from increased amino acid catabolism. Studying AD from a metabolic perspective provides new insights into AD pathogenesis and may lead to the discovery of dietary metabolite supplements that can partially compensate for alterations of enzymatic function to delay AD or alleviate some of the suffering caused by the disease.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1155/2017/5472792

Cites

139 of 139 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Neurons could use glucogenic or ketogenic amino acids to generate TCA intermediates to produce ATP through oxidative phosphorylation when glucose is scarce.

    “Neurons could also use glucogenic or even ketogenic amino acids to generate TCA intermediates to produce ATP through oxidative phosphorylation when glucose is scarce [128].”

    From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [128]

    Section 5 says that amino acid catabolism likely helps AD neurons maintain ATP when glucose metabolism declines, and Section 4.4 says branched-chain amino acid carbons can enter the citric acid cycle. The paper does not explicitly distinguish glucogenic from ketogenic amino acids in this pathway, and its discussion concerns impaired glucose metabolism in AD rather than glucose scarcity in neurons generally. Page numbers were not available in our copy. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Griffin, J. W. D., & Bradshaw, P. C.
Affiliations
East Tennessee State University (US)
Corresponding author
Bradshaw, Patrick C.
Venue
Oxidative Medicine and Cellular Longevity
Publisher
Wiley
Published
2017-01
Volume
2017
Issue
1
Pages
5472792-5472792
ISSN
  • 1942-0994 (ISSN-L)
  • 1942-0900
OpenAlex
W2584342410
Cited by
185
References
139
Citations by year
2026: 15 · 2025: 24 · 2024: 26 · 2023: 24 · 2022: 25 · 2021: 20 · 2020: 25 · 2019: 14 · 2018: 10 · 2017: 2
FWCI
1.71
Type
journal article
Language
en
Open access
Locations
  • Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Digital Commons - East Tennessee State University (East Tennessee State University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, amino acid catabolism, amino acid oxidation, brain energy homeostasis, urea cycle, ammonia detoxification, endothelial cells, pathogenesis, therapeutic target
MeSH terms
Alzheimer Disease, Amino Acids, Animals, Brain, Homeostasis, Humans, Metabolism, Neurons

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review