# Immediate and Long-Term Effectiveness of a Therapeutic Exercise Protocol in Patients with Dementia

**Authors:** Ferreira-Sánchez María del Rosario, García-Macías Celia, Alarcón-Jiménez Jorge, Martín Jiménez Ana, Gómez-Sánchez Sonia, De Bernardo Nieves, Sánchez-Jiménez Elena

PMC · DOI: 10.3390/jcm15041482 · 2026-02-13

## TL;DR

A structured exercise program can help slow physical decline in dementia patients, both immediately and over time.

## Contribution

This study evaluates the short- and medium-term effects of a monitored therapeutic exercise program on motor function in dementia patients.

## Key findings

- The exercise program improved general motor function, balance, trunk control, and mobility in dementia patients.
- Functional improvements were maintained for up to 6 months after the program ended.
- No significant improvement was observed in independence for daily living activities.

## Abstract

Background/Objectives: Therapeutic exercise (TE) has been shown to be an effective tool for slowing physical and cognitive decline in patients with dementia. However, its true impact on physical and functional variables, as well as the duration of its effects once therapy is discontinued, remains unclear. The aim was to analyze the short- and medium-term effects of a structured and monitored TE program on motor function in patients with dementia. Methods: A pre–post clinical trial was conducted in individuals with a medical diagnosis of mild-to-moderate cognitive impairment (Mini-Mental State Examination scores between 10 and 23) who had not engaged in regular exercise during the previous 6 months. The study variables and their measurement tools included general motor function (Short Physical Performance Battery), trunk control (Trunk Control Test), balance (Berg Balance Scale), overall mobility and gait (Timed Up and Go Test), and degree of independence in activities of daily living (ADLs) (Barthel Index). Participants completed a 12-week TE intervention at moderate intensity, 3 days per week for 45 min sessions. The program included aerobic training and strength, coordination, flexibility, and balance exercises. TE intensity was monitored through heart rate and dynamic maximal resistance. Assessments were conducted at baseline (t0), immediately after the program (t1), and 6 months after completion (t2). Results: Significant global longitudinal effects of time were observed for general motor function, balance, trunk control, and mobility and gait, whereas no significant global effect was detected for independence in activities of daily living. Post-intervention changes were non-significant; however, several pairwise comparisons showed moderate-to-large effect sizes. Follow-up assessments revealed shifts in performance distributions consistent with functional decline. Conclusions: A structured TE program performed at moderate intensity may help slow or attenuate the physical decline experienced by individuals with dementia.

## Linked entities

- **Diseases:** dementia (MONDO:0001627)

## Full-text entities

- **Genes:** FNDC5 (fibronectin type III domain containing 5) [NCBI Gene 252995] {aka FRCP2, irisin}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, IL24 (interleukin 24) [NCBI Gene 11009] {aka C49A, FISP, IL10B, MDA7, MOB5, ST16}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CTSB (cathepsin B) [NCBI Gene 1508] {aka APPS, CPSB, KWE, RECEUP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, BBS2 (Bardet-Biedl syndrome 2) [NCBI Gene 583] {aka BBS, RP74}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** Musculoskeletal or cardiovascular comorbidities (MESH:D009140), embolism (MESH:D004617), sinus tachycardia (MESH:D013616), depression (MESH:D003866), atrial or ventricular arrhythmias (MESH:D001145), chest pain (MESH:D002637), fatigue (MESH:D005221), acute stroke (MESH:D020521), muscle aches (MESH:D063806), Dementia (MESH:D003704), multiple sclerosis (MESH:D009103), thrombophlebitis (MESH:D013924), brain fog (MESH:D005222), Cognitive decline (MESH:D003072), unstable angina (MESH:D000789), Cardiorespiratory sequelae (MESH:D000094024), inflammatory (MESH:D007249), injury to (MESH:D014947), MCID (MESH:D000076263), loss of autonomy (MESH:D016388), death (MESH:D003643), deterioration of physical (MESH:D059445), fractures (MESH:D050723), mobility decline (MESH:D014086), PD (MESH:D010300), hip fracture (MESH:D006620), dyspnea (MESH:D004417), neuropsychiatric symptoms (MESH:D001523), AD (MESH:D000544), MCI (MESH:D060825), SARS-CoV-2 infection (MESH:D000086382), neuropsychiatric (MESH:C000631768), knee osteoarthritis (MESH:D020370), cough (MESH:D003371), anxiety (MESH:D001007)
- **Chemicals:** ketone bodies (MESH:D007657), glucose (MESH:D005947), Pilates (-), lactate (MESH:D019344), cortisol (MESH:D006854)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941492/full.md

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Source: https://tomesphere.com/paper/PMC12941492