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Glycolipids are dominant glycans in vertebrate brains. Complex gangliosides GD1a, GD1b and GT1b are ubiquitously expressed on neurons while GM1 is marker of fibers in all reptilian, bird and mammalian brains. Complete lack of complex gangliosides does not interrupt brain morphogenesis but does affect long term myelin and axon maintenance due to interaction of GD1a and GT1b with oligodendrocyte ligand MAG. The same axon/myelin preserving interaction turns into regeneration obstructing in the case of injury in adult brain. In contrast to higher vertebrates, fish and amphibian brains are deficient in complex gangliosides but well known as regeneration-competent. Using antibodies for GM1, GD1a, GD1b and GT1b we investigated difference in distribution of gangliosides in brains of sturgeon (Fig. 1), catfish (Fig. 2), carp (Fig. 3), trout (Fig. 4), pike (Fig. 5) and perch (Fig. 6). Contrary to other vertebrates that have uniform pattern of ganglioside expression, investigated species of Actinopterygii varied in ganglioside expression. All but one species (sturgeon) expressed GM1 as neuronal marker, not being present on fibers like in mammalian brain. Catfish, carp and trout express GM1 and GT1b on individual neurons in telencephalon, hypothalamic nucleai, granular neurons in cerebellum and stratum periventriculare in optic tectum. GD1a is almost undetectable in trout, GD1b in catfish and carp while GT1b in perch brain. Brain of sturgeon has expression of complex gangliosides resembling one observed in higher vertebrates and its regeneration-competence could be farther investigated.

The neural cell adhesion molecule (NCAM) plays important role in adult neurogenesis, survival and migration of neuronal steam cells. Reversible attachment of polysialc acid (PSA) to extra cellular domain of NCAM promotes migration which is limited to rostral olfactory stream in the adult brain of mammals. Non-mammalian vertebrates poses much higher potential for regeneration due to constitutive adult neurogenesis, apoptotic elimination of damaged cells and efficient migration, differentiation and integration of newly derived cells in existing neural network. We compared expression of PSA-NCAM in sturgeon (Acipenser ruthenus), carp (Cyprinus carpio), trout (Salmo gairdneri), catfish (Silurus glanis), perch (Perca fluviatilis) and pike (Esox lucius) brains with two different antibodies (mAb735 and clone 2-2B). PSA-NCAM zones in carp, trout and perch brain extend from telencephalon into cerebellum and mesencephalon. From the level of rostral mesencephalon toward spinal cord extensive PSA-NCAM zone exist in sturgeon and pike brain. While two antibodies give similar result on trout and pike brains, reactivity of mAb735 is limited to cerebellar proliferation zone in perch and carp. Also, carp and catfish brain, contrary to others, have proliferative zones in facial and vagal lobes - enlargement of nucleus solitarius connected with taste system and specialized palatal organ. PSA-NCAM is just one of the markers that are indicating potential for regeneration, but its expression in rhombencephalon and spinal cord of sturgeon and pike could be promising for spinal cord injury studies.

Objective: To identify clinical and psychometric indicators that distinguishes Alzheimer’ s dementia (AD) and frontotemporal lobar degeneration (FTLD), confirmed at autopsy, at initial presentation. Background: FTLD is a focal, non-Alzheimer form of dementia clinically characterized as either behavioral or aphasic variants, without amnestic syndrome, at least in the early stage of the disease (1, 2). Compared to individuals with AD, overall survival amongst those affected with FTLD is shorter (3). A proportion of patients who meet clinical criteria for AD have FTLD confirmed at autopsy, with or without neuropathological AD (4). Thus, the clinical phenotypes of the two disorders may overlap. Methods: A retrospective review of 48 neuropathologically confirmed cases of FTLD (27 had completed psychometric testing) yielded clinical and neuropsychological features for comparison with 27 age-, sex-, education-, and severity-matched individuals with AD. Results At first visit, FTLD differed from AD by behavioral abnormalities, particularly disinhibition and impulsivity, less social withdrawal, and progressive nonfluent aphasia. The two diseases had comparable executive dysfunction and memory problems. The FTLD individuals performed better than those with AD on a visual test of episodic memory, but worse on word fluency (performance correlated with aphasic features). Histopathological AD was present in 11 of the 48 FTLD individuals. Conclusions The clinical and cognitive features of FTLD may overlap with AD, particularly for memory and executive function, although behavioral problems and language difficulties distinguish those with FTLD (3, 5). FTLD individuals were more impaired than those with AD on a word fluency task, but less impaired on tests of nonverbal memory. Memory complaints in FTLD may in part reflect word-finding difficulties stemming from language dysfunction (2). Compounding the overlap of FTLD and AD clinical phenotypes is the presence of neuropathological AD in almost one-fourth of FTLD individuals. References: 1. Neary D, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 1998 ; 51: 1546-1554. 2. Liscic RM, et al. Clinical and psychometric distinction of frontotemporal and Alzheimer dementias. Arch Neurol 2007 ; 64: 535-540. 3. Rosen HJ, et al. Utility of clinical criteria in differentiating frontotemporal lobar degeneration (FTLD) from AD. Neurology 2002 ; 58: 1608-1615. 4. Varma AR, et al. Evaluation of the NINCDS-ADRDA criteria in the differentiation of Alzheimer’ s disease and frontotemporal dementia. J Neurol Neurosurg Psychiatry 1999 ; 66: 184-188. 5. Rascovsky K, et al. Cognitive profiles differ in autopsy-confirmed frontotemporal dementia and AD. Neurology 2002 ; 58: 1801-1808.