Background and Aims: Alzheimer's disease (AD), primarily characterized by cognitive impairment, places an immense burden on patients and caregivers. Non‐invasive neuromodulation with repetitive transcranial magnetic stimulation has been proposed to improve cognition in mild to moderate AD. This narrative review aimed to summarize clinical trial evidence on the effects, safety, and tolerability of rTMS for AD‐related cognitive impairment and to identify research gaps. Methods: A narrative review of clinical trials was performed. PubMed/MEDLINE, Embase, Cochrane Google scholar, and Scopus were searched from inception to January 25, 2025, using terms for “repetitive transcranial magnetic stimulation”, “Alzheimer's disease”, “cognitive impairment”, “clinical trials”, and “randomized controlled trial”. Clinical trials of active rTMS versus sham or treatment‐as‐usual in adults with mild to moderate AD that reported validated cognitive outcomes were included. Data on rTMS protocols, cognitive measures, adverse effects, and follow‐up were extracted and synthesized narratively without statistical pooling. Results: 14 trials were included. Across most studies, rTMS delivered at 5–20 Hz for 4 to 12 weeks, at least 5 days per week, was associated with improved cognitive function. Improvements were reported on tools such as the MMSE, CDR‐SB, SIB, and ADAS‐Cog, with statistically significant differences versus sham in most trials [ p < 0.05], and some evidence of sustained benefit at follow‐up. rTMS was generally safe and tolerable. Reported adverse effects were mild to moderate and included transient headache, scalp or skin discomfort, pain, and fatigue. Preliminary evidence also suggested potential neuropsychiatric benefits. However, substantial heterogeneity in duration, frequency, treatment plan, targets, and outcome measures limited definitive conclusions. Conclusion: rTMS appears safe in the short term and may be linked to short‐term cognitive and neuropsychiatric gains in mild to moderate AD. However, marked protocol heterogeneity, small sample sizes, short follow‐up, and risk of bias limit certainty and prevent identification of optimal parameters. rTMS is not ready for routine AD care. Larger, sham‐controlled trials with standardized protocols and biomarker or long‐term outcomes are needed.

Amyotrophic lateral sclerosis (ALS) is a progressive, fatal neurodegenerative disease primarily affecting upper and lower motor neurons. Although cerebrovascular disease (CVD) and ALS have traditionally been studied as distinct entities, a growing body of evidence indicates meaningful epidemiological, pathophysiological, and clinical overlap between the two conditions. This narrative review synthesizes current evidence on the coexistence of ALS and cerebrovascular disease, examines shared mechanistic pathways, addresses diagnostic challenges, including stroke mimicry, considers clinical management implications, and identifies priorities for future research. A search of PubMed, Scopus, Web of Science, and EMBASE was conducted through February 2026 using the terms “amyotrophic lateral sclerosis,” “motor neuron disease,” “cerebrovascular disease,” “stroke,” “ischemic stroke,” “blood-brain barrier,” “neuroinflammation,” and “neurovascular coupling,” alone and in combination. Peer-reviewed original research, systematic reviews, meta-analyses, population-based studies, registry analyses, and expert consensus statements were included. Studies were assessed for methodological quality and relevance to the review objectives. This review is reported as a narrative synthesis. Population-based data demonstrate a bidirectional relationship between ALS and cerebrovascular events. ALS patients face an approximately 2.6-fold elevated risk of ischemic stroke, and prior cerebrovascular injury modestly increases subsequent ALS risk. Shared pathophysiological mechanisms include neuroinflammation with microglial M1/M2 polarization imbalance, pro-inflammatory cytokine cascades mediated via NF-κB signaling, oxidative stress and SOD1 pathway dysregulation, glutamate excitotoxicity, blood–brain barrier (BBB) dysfunction, and impaired neurovascular coupling. Diagnostic confusion arises because upper motor neuron–predominant ALS can closely mimic acute ischemic stroke. Concurrent cerebrovascular disease appears to accelerate functional decline and reduce survival in ALS. Resource-limited settings face compounded challenges from diagnostic misclassification, restricted EMG access, and limited specialist availability. The ALS–cerebrovascular overlap is clinically relevant, biologically plausible, and systematically understudied. Integrated multidisciplinary management, prospective longitudinal cohort studies, and linked registry analyses are urgently needed to clarify causal relationships, characterize shared disease mechanisms, and improve patient outcomes.