Scoping review maps NPY, autophagy and brain ageing evidence
A scoping review of four studies found that in a progeroid mouse model NPY levels decline in the hypothalamic arcuate nucleus and restoring NPY delays several ageing phenotypes; NPY may mitigate brain ageing by promoting autophagy via PI3K/AKT/mTOR suppression and ERK1/2-MAPK activation. [1]
Automatic summary · not editorially reviewed
The key findings
The scoping review systematically screened studies published between 2014 and 2026 and included four articles meeting its criteria. [1]
In a progeroid mouse model, NPY levels decline in the hypothalamic arcuate nucleus, and restoring NPY delays several ageing phenotypes. [1]
NPY appears to mitigate brain ageing by promoting autophagy in the hypothalamus and cerebral cortex, requiring PI3K/AKT/mTOR suppression and ERK1/2-MAPK activation. [1]
The source at a glance
- Study type / format
- Scoping review of four studies (abstract)
- Population / context
- Studies of neuropeptide Y, autophagy and brain ageing, including a progeroid mouse model
- Summary based on
- Study abstract
- Original publication
- September 21, 2026
NPY and age-related brain dysfunction evidence map
The review asks how far neuropeptide Y (NPY) contributes to brain ageing, focusing on autophagy, a cellular recycling mechanism involved in brain ageing. Studies published between 2014 and 2026 were systematically screened; after a rigorous selection process, four articles met the inclusion and exclusion criteria and were analysed. The authors state that the extent of NPY's contribution remains unclear.
Supporting source [1]
Progeroid mouse model: NPY decline and delayed phenotypes
In a progeroid mouse model, NPY levels decline in the hypothalamic arcuate nucleus, and restoring NPY delays several ageing phenotypes. The review further reports that NPY appears to mitigate brain ageing by promoting autophagy in the hypothalamus and cerebral cortex, an effect requiring both suppression of PI3K/AKT/mTOR signalling and activation of ERK1/2-MAPK. These are findings from the included studies, not established human outcomes.
Supporting source [1]
Open mechanisms and future research directions
The authors say further investigation is needed to clarify how NPY acts, including the roles of its various receptors and its interactions with other neuropeptides. They suggest the insights may pave the way for future research into therapeutic strategies targeting NPY against age-related cognitive deficits and neurodegenerative diseases; this is a research outlook, not a demonstrated treatment.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The review included just four articles, and the reported findings come from a progeroid mouse model and mechanistic work, not from human studies. The authors state that NPY's contribution to brain ageing remains unclear and that receptor roles and interactions with other neuropeptides need further investigation.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Cheah SY, Kumari Y, Mohd Sahardi NFN, Saud Gany SL, Abdullah NAH, Makpol S, Jaafar F. · europepmc.org · September 21, 2026