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Basic Science and Pathogenesis.
Namrata Kumari1, Maggie Sodders1, Archana Marathi1
1University of Pittsburgh, Pittsburgh, PA, USA.
Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
Summary
Adenylate kinase 1 (Ak1) deficiency shows neuroprotective effects in an alpha-synucleinopathy mouse model. Ak1 knockout mice exhibit reduced reactive astrocytes and alpha-synuclein levels, suggesting Ak1 as a therapeutic target for dementia with Lewy bodies.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Dementia with Lewy bodies (DLB) is a prevalent neurodegenerative disorder.
- Current disease-modifying therapies for DLB are limited.
- Glial cells play a role in alpha-synucleinopathies.
Purpose of the Study:
- To investigate the neuroprotective role of adenylate kinase 1 (Ak1) in an alpha-synucleinopathy model.
- To validate Ak1 as a potential therapeutic target for DLB.
Main Methods:
- Utilized Ak1 knockout (Ak1-/-) mice and wild-type littermates.
- Administered adeno-associated virus carrying alpha-synuclein (AAV2-α-synuclein) via stereotactic injection.
- Assessed neuroinflammation (reactive astrocytes, microglia), alpha-synuclein pathology, and dopaminergic neuron loss at multiple time points.
Main Results:
- Ak1-/- mice showed reduced reactive astrocytes (GFAP expression) at 1 and 3 months post-injection.
- Decreased levels of total and phosphorylated alpha-synuclein were observed in Ak1-/- mice.
- Preliminary behavioral data and dopaminergic neuron counts were assessed.
Conclusions:
- Ak1 deficiency confers protection against alpha-synuclein-induced pathology in mice.
- Reduced neuroinflammation and alpha-synuclein accumulation in Ak1-/- mice support its therapeutic potential.
- Ak1 is a promising glial-based therapeutic target for alpha-synucleinopathies like DLB.
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