Diabetic peripheral neuropathy (DPN) increases fall risk in diabetics. Due to varying variables used to assess fall risk, the impact of exercise on fall prevention remains inconsistent. This study reviews and compares the effects of different exercises on fall risk among older adults with DPN. A comprehensive literature search was conducted in PubMed, EBSCO, Web of Science, and Cochrane Library up to February 17th, 2025. Inclusion criteria were: older adults with DPN; exercise intervention only, an inactive or non-exercising control group, and randomized controlled trials with outcome variables: timed up and go (TUG) time, gait speed, Berg Balance Scale (BBS) score, one-legged standing (OLS) time with eye open (EO) and closed (EC). The mean difference (MD) and 95 % confidence interval (CI) were calculated. A total of 21 articles included five exercise types: balance exercise (BE), multi-component exercise (ME), strength exercise (SE), whole-body vibration (WBV) and foot-ankle functional training (FT). BE reduced TUG time (MD = −1.47, 95 % CI = −1.79 to −1.15) and increased gait speed (0.11, 0.04–0.18), BBS score (0.93, 0.49–1.37), and OLS time (EO: 2.72, 1.86–3.58; EC:1.58, 1.0–2.17). ME reduced TUG time (−1.71, −2.26 to −1.17) and increased BBS score (2.0, 1.28–2.72) and OLS time (EO: 7.07, 4.35–9.79; EC: 2.61, 1.28–3.94); SE reduced TUG time (−1.45, −2.75 to −0.15) and increased gait speed (0.09, 0.06–0.12); WBV increased OLS time (EO: 1.94, 1.32–2.56; EC: 1.86, 0.16–3.56) but did not affect TUG time or gait speed. FT did not affect TUG time or gait speed. Exercise reduced fall risks among older adults with DPN. BE and ME were effective in reducing fall risks, followed by SE. WBV improved static balance but failed in dynamic balance. FT showed limited effects on fall prevention and was not recommended.

Parkinson’s disease (PD) is characterized by progressive degeneration of the nigrostriatal dopaminergic system and α-synuclein (α-syn) pathology, with disease progression driven by convergent mechanisms including neuroinflammation, mitochondrial injury, oxidative stress, and regulated cell-death programs such as ferroptosis. Fibroblast growth factors (FGFs) and fibroblast growth factor receptors (FGFRs) constitute a key signaling system in the central nervous system, influencing not only neuronal survival and glial states but also intersecting with networks governing redox homeostasis and iron metabolism. Accumulating evidence indicates that, beyond classical neurotrophic actions, FGF–FGFR signaling can modulate mitochondrial quality control, glial inflammatory activation, and lipid peroxidation-related processes, thereby reshaping cellular susceptibility to ferroptotic injury. This review summarizes current advances in understanding FGF signaling networks in Parkinson’s disease, synthesizes their potential mechanistic links to the interplay among neuroinflammation, mitochondrial dysfunction, and redox imbalance as well as to ferroptosis regulation, and discusses the experimental basis and translational challenges of targeting the FGF pathway as a disease-modifying therapeutic strategy.