INTRODUCTION: Cognitive impairment is a major contributor to disability in Parkinson’s disease (PD) and Alzheimer’s disease (AD). Neurophysiologically, AD is characterized by early hippocampal and temporoparietal cortical degeneration associated with amyloid-β and tau pathology, producing prominent episodic memory deficits. In PD, cognitive decline arises primarily from dopaminergic depletion and α-synuclein-related disruption of fronto-striatal and cholinergic networks, leading initially to executive, attentional, and visuospatial dysfunction.

AIM(S): To synthesize evidence published between 2010 and 2025 from Scopus, PubMed, and Google Scholar on the prevalence, cognitive profiles, progression, and determinants of cognitive impairment in PD and AD, with emphasis on comparative findings and epidemiological estimates.

METHOD(S): A narrative review of clinical, epidemiological, and longitudinal studies addressing mild cognitive impairment (MCI), dementia, and domain-specific cognitive deficits in PD and AD. Eligible articles published from 2010 to 2025 were screened and analyzed qualitatively.

RESULTS: Evidence across studies indicates that cognitive impairment is common in both disorders but differs in presentation and evolution. In PD, mild cognitive impairment is observed in approximately 20–35% of patients near the time of diagnosis, while longitudinal cohorts report a cumulative dementia risk ranging from about 40% to 80% over 10 to 20 years. In the AD spectrum, amnestic MCI represents a frequent prodromal stage, with annual conversion rates to AD dementia typically estimated between 10% and 20%, particularly among biomarker-positive individuals. The cognitive phenotype in PD is dominated by deficits in executive function, attention, and visuospatial processing, whereas AD is characterized by early and marked impairment of episodic memory followed by language and visuoconstructive decline. Neurobiological correlates further differentiate the conditions, as PD-related cognitive deterioration is associated with cholinergic denervation, cortical Lewy body pathology, and altered fronto-striatal connectivity, while AD progression is linked to amyloid and tau accumulation, hippocampal atrophy, and temporoparietal hypometabolism. Shared modifiers of accelerated decline include advanced age, lower educational attainment, vascular comorbidities, depression, and sleep disturbances.

CONCLUSIONS: Literature from 2010–2025 confirms that although PD and AD frequently progress toward dementia, they exhibit distinct early cognitive signatures and underlying neurophysiological mechanisms. These differences are critical for early diagnosis, prognostic assessment, and development of targeted therapeutic and cognitive interventions.

FINANCIAL SUPPORT: no