Parkinsonism may be a clinical manifestation of a wide range of disease entities, and still poses a great diagnostic challenge. In an attempt to provide further insight into the differential diagnosis of PD versus progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), and Lewy body dementia (LBD), several biomarkers have been investigated, yielding inconclusive results, OCT being among them. The present review aims to explore the potential diagnostic value of evaluating retinal parameters through OCT implementation among patients presenting with a Parkinsonian syndrome, with an emphasis on effective differentiation between distinct syndromes. Having reviewed all the available literature published within the last decade, neurodegeneration seems to be paralleled with degeneration and alterations of the retina that may be quantified by OCT. Specific patterns of structural changes within the retina may provide valuable information on the underlying pathology, thus highlighting the role of OCT as a diagnostic tool within this group of patients. Although still not utilized in clinical practice, OCT, if further explored and validated, may significantly enhance overall Parkinsonism care.

Within the phenotypic spectrum of Alzheimer’s disease (AD), Creutzfeldt–Jakob disease (CJD) and cerebral amyloid angiopathy (CAA), dementia that is attributed to iatrogenic transmission has increasingly gained scientific attention recently. Newly recognized, this treatment-induced form of dementia may result from exposure to certain medical or surgical procedures. The present review aims to explore the distinct features of acquired dementia encompassing a history of potential exposure and relatively early age of onset, highlighting transmission potential with a rather prion-like pattern. Having reviewed all available relevant literature, dementia of iatrogenic etiology represents a new disease entity that requires an individualized investigation process and poses a great clinical challenge as far as patients with AD, CJD and CAA are concerned. Understanding the underlying pathophysiology of these rare forms of dementia may significantly enhance awareness within clinical field of neurodegenerative diseases and facilitate their prompt management.

Eating behavior disturbances are increasingly recognized as clinically relevant features of dementias. Although underappreciated, such alterations affect nutritional status, metabolic state, and disease burden. Alzheimer’s disease (AD) and frontotemporal lobar degeneration (FTLD) exhibit a wide range of manifestations in eating and appetite regulation. In behavioral variant frontotemporal dementia (bvFTD), hyperorality, increased appetite, preference for sweet and high-fat foods, altered table manners, and consumption of inedible objects are common and may appear early. In contrast, AD patients usually present with decreased appetite, early dysphagia, and weight loss, although increased appetite may also occur. Beyond clinical manifestations, this review synthesizes current evidence regarding the prevalence, metabolic and hormonal profiles, and neuroimaging patterns of eating behavior disturbances in FTLD and AD, provides insight into the complex underlying mechanisms causing these changes, and underlines the lack of clear treatment strategies in these cases.

The diagnosis of behavioral variant of frontotemporal dementia (bvFTD)—a common cause of early-onset dementia—remains challenging due to a lack of determined biomarkers. 18F-fluorodeoxyglucose-positron emission tomography (FDG–PET) scan detects early glucose metabolism alterations in specific brain regions. The detection of distinct hypometabolic patterns in early stages of bvFTD has established FDG–PET as an indispensable adjunctive diagnostic tool in inconclusive cases, as well as in distinguishing between different types of dementia. Moreover, its role in the differential diagnosis of the often overlapping bvFTD and primary psychiatric disorders (PPD) is being studied by exploring disease-specific hypometabolic areas. Finally, the identification of early metabolic alterations and even earlier alterations in distinct metabolic brain networks may assist the diagnosis of presymptomatic carriers of disease-related gene mutations and lead to the development of novel biomarkers. The aim of our review is to underscore the role of FDG–PET as an approved yet promising tool that may lead to a new era in the diagnosis of bvFTD by establishing novel biomarkers and integrating AI as an assistant modality to inform diagnosis and decision-making.